Key publications in HIV-Aging research

@article{murzin_we_2022,
	title = {\textit{“{We} can hardly even do it nowadays. {So}, what's going to happen in 5 years from now, 10 years from now?”} {The} health and community care and support needs and preferences of older people living with {HIV} in {Ontario}, {Canada}: a qualitative study},
	volume = {25},
	issn = {1758-2652, 1758-2652},
	shorttitle = {{\textless}i{\textgreater}“{We} can hardly even do it nowadays. {So}, what's going to happen in 5 years from now, 10 years from now?},
	url = {https://onlinelibrary.wiley.com/doi/10.1002/jia2.25978},
	doi = {10.1002/jia2.25978},
	language = {en},
	number = {S4},
	urldate = {2022-11-22},
	journal = {Journal of the International AIDS Society},
	author = {Murzin, Kate and Racz, Elizabeth and Behrens, D. M. and Conway, Tracey and Da Silva, George and Fitzpatrick, Eimear and Lindsay, Joanne D. and Walmsley, Sharon L. and {the PANACHE study team}},
	month = sep,
	year = {2022},
}

@article{farley_progress_2022,
	title = {Progress towards the {UNAIDS} 90‐90‐90 targets among persons aged 50 and older living with {HIV} in 13 {African} countries},
	volume = {25},
	issn = {1758-2652, 1758-2652},
	url = {https://onlinelibrary.wiley.com/doi/10.1002/jia2.26005},
	doi = {10.1002/jia2.26005},
	language = {en},
	number = {S4},
	urldate = {2022-11-22},
	journal = {Journal of the International AIDS Society},
	author = {Farley, Shannon M. and Wang, Chunhui and Bray, Rachel M. and Low, Andrea Jane and Delgado, Stephen and Hoos, David and Kakishozi, Angela N. and Harris, Tiffany G. and Nyirenda, Rose and Wadonda, Nellie and Li, Michelle and Amuri, Mbaraka and Juma, James and Kancheya, Nzali and Pietersen, Ismela and Mutenda, Nicholus and Natanael, Salomo and Aoko, Appolonia and Ngugi, Evelyn W. and Asiimwe, Fred and Lecher, Shirley and Ward, Jennifer and Chikwanda, Prisca and Mugurungi, Owen and Moyo, Brian and Nkurunziza, Peter and Aibo, Dorothy and Kabala, Andrew and Biraro, Sam and Ndagije, Felix and Musuka, Godfrey and Ndongmo, Clement and Shang, Judith and Dokubo, Emily K. and Dimite, Laura E. and McCullough‐Sanden, Rachel and Bissek, Anne‐Cecile and Getaneh, Yimam and Eshetu, Frehywot and Nkumbula, Tepa and Tenthani, Lyson and Kayigamba, Felix R. and Kirungi, Wilford and Musinguzi, Joshua and Balachandra, Shirish and Kayirangwa, Eugenie and Ayite, Ayayi and West, Christine A. and Bodika, Stephane and Sleeman, Katrina and Patel, Hetal K. and Brown, Kristin and Voetsch, Andrew C. and El‐Sadr, Wafaa M. and Justman, Jessica E.},
	month = sep,
	year = {2022},
}

@article{luk_sarcopenia_2022,
	title = {Sarcopenia in people living with {HIV} in {Hong} {Kong}: which definition correlates with health outcomes?},
	volume = {25},
	issn = {1758-2652, 1758-2652},
	shorttitle = {Sarcopenia in people living with {HIV} in {Hong} {Kong}},
	url = {https://onlinelibrary.wiley.com/doi/10.1002/jia2.25988},
	doi = {10.1002/jia2.25988},
	language = {en},
	number = {S4},
	urldate = {2022-11-22},
	journal = {Journal of the International AIDS Society},
	author = {Luk, Fion Wing Lam and Li, Timothy and Ho, Hang Yee and Chan, Yin Yan and Cheung, Siu King and Wong, Vickie and Kwok, Timothy Chi Yui and Lui, Grace},
	month = sep,
	year = {2022},
}

@article{aurpibul_neurocognitive_2022,
	title = {Neurocognitive performance and quality of life of older adults with {HIV} on antiretroviral treatment in {Northern} {Thailand}},
	volume = {25},
	issn = {1758-2652, 1758-2652},
	url = {https://onlinelibrary.wiley.com/doi/10.1002/jia2.25983},
	doi = {10.1002/jia2.25983},
	language = {en},
	number = {S4},
	urldate = {2022-11-22},
	journal = {Journal of the International AIDS Society},
	author = {Aurpibul, Linda and Sripan, Patumrat and Tangmunkongvorakul, Arunrat and Chaikan, Wilawan and Sarachai, Saowalak and Srithanaviboonchai, Kriengkrai},
	month = sep,
	year = {2022},
}

@article{noauthor_issue_2022,
	title = {Issue {Information}},
	volume = {25},
	issn = {1758-2652, 1758-2652},
	url = {https://onlinelibrary.wiley.com/doi/10.1002/jia2.26010},
	doi = {10.1002/jia2.26010},
	language = {en},
	number = {S4},
	urldate = {2022-11-22},
	journal = {Journal of the International AIDS Society},
	month = sep,
	year = {2022},
}

@article{lam_comparison_2022,
	title = {Comparison of dementia incidence and prevalence between individuals with and without {HIV} infection in primary care from 2000 to 2016},
	volume = {36},
	issn = {0269-9370, 1473-5571},
	url = {https://journals.lww.com/10.1097/QAD.0000000000003134},
	doi = {10.1097/QAD.0000000000003134},
	language = {en},
	number = {3},
	urldate = {2022-11-22},
	journal = {AIDS},
	author = {Lam, Jennifer O. and Lee, Catherine and Gilsanz, Paola and Hou, Craig E. and Leyden, Wendy A. and Satre, Derek D. and Flamm, Jason A. and Towner, William J. and Horberg, Michael A. and Silverberg, Michael J.},
	month = mar,
	year = {2022},
	pages = {437--445},
}

@article{thames_racial_2022,
	title = {Racial differences in health and cognition as a function of {HIV} among older adults},
	volume = {36},
	issn = {1385-4046, 1744-4144},
	url = {https://www.tandfonline.com/doi/full/10.1080/13854046.2021.1967449},
	doi = {10.1080/13854046.2021.1967449},
	language = {en},
	number = {2},
	urldate = {2022-11-22},
	journal = {The Clinical Neuropsychologist},
	author = {Thames, April D. and Nunez, Rodolfo and Slavich, George M. and Irwin, Michael R. and Senturk, Damla},
	month = feb,
	year = {2022},
	pages = {367--387},
}

@article{montano_biological_2022,
	title = {Biological ageing with {HIV} infection: evaluating the geroscience hypothesis},
	volume = {3},
	issn = {26667568},
	shorttitle = {Biological ageing with {HIV} infection},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S2666756821002786},
	doi = {10.1016/S2666-7568(21)00278-6},
	language = {en},
	number = {3},
	urldate = {2022-11-22},
	journal = {The Lancet Healthy Longevity},
	author = {Montano, Monty and Oursler, Krisann K and Xu, Ke and Sun, Yan V and Marconi, Vincent C},
	month = mar,
	year = {2022},
	pages = {e194--e205},
}

@article{horvath_hiv_2022,
	title = {{HIV}, pathology and epigenetic age acceleration in different human tissues},
	volume = {44},
	issn = {2509-2715, 2509-2723},
	url = {https://link.springer.com/10.1007/s11357-022-00560-0},
	doi = {10.1007/s11357-022-00560-0},
	abstract = {Abstract 
            Epigenetic clocks based on patterns of DNA methylation have great importance in understanding aging and disease; however, there are basic questions to be resolved in their application. It remains unknown whether epigenetic age acceleration (EAA) within an individual shows strong correlation between different primary tissue sites, the extent to which tissue pathology and clinical illness correlate with EAA in the target organ, and if EAA variability across tissues differs according to sex. Considering the outsized role of age-related illness in Human Immunodeficiency Virus-1 (HIV), these questions were pursued in a sample enriched for tissue from HIV-infected individuals. We used a custom methylation array to generate DNA methylation data from 661 samples representing 11 human tissues (adipose, blood, bone marrow, heart, kidney, liver, lung, lymph node, muscle, spleen and pituitary gland) from 133 clinically characterized, deceased individuals, including 75 infected with HIV. We developed a multimorbidity index based on the clinical disease history. Epigenetic age was moderately correlated across tissues. Blood had the greatest number and degree of correlation, most notably with spleen and bone marrow. However, blood did not correlate with epigenetic age of liver. EAA in liver was weakly correlated with EAA in kidney, adipose, lung and bone marrow. Clinically, hypertension was associated with EAA in several tissues, consistent with the multiorgan impacts of this illness. HIV infection was associated with positive age acceleration in kidney and spleen. Male sex was associated with increased epigenetic acceleration in several tissues. Preliminary evidence indicates that amyotrophic lateral sclerosis is associated with positive EAA in muscle tissue. Finally, greater multimorbidity was associated with greater EAA across all tissues. Blood alone will often fail to detect EAA in other tissues. While hypertension is associated with increased EAA in several tissues, many pathologies are associated with organ-specific age acceleration.},
	language = {en},
	number = {3},
	urldate = {2022-11-22},
	journal = {GeroScience},
	author = {Horvath, Steve and Lin, David T. S. and Kobor, Michael S. and Zoller, Joseph A. and Said, Jonathan W. and Morgello, Susan and Singer, Elyse and Yong, William H. and Jamieson, Beth D. and Levine, Andrew J.},
	month = jun,
	year = {2022},
	pages = {1609--1620},
}

Abstract Epigenetic clocks based on patterns of DNA methylation have great importance in understanding aging and disease; however, there are basic questions to be resolved in their application. It remains unknown whether epigenetic age acceleration (EAA) within an individual shows strong correlation between different primary tissue sites, the extent to which tissue pathology and clinical illness correlate with EAA in the target organ, and if EAA variability across tissues differs according to sex. Considering the outsized role of age-related illness in Human Immunodeficiency Virus-1 (HIV), these questions were pursued in a sample enriched for tissue from HIV-infected individuals. We used a custom methylation array to generate DNA methylation data from 661 samples representing 11 human tissues (adipose, blood, bone marrow, heart, kidney, liver, lung, lymph node, muscle, spleen and pituitary gland) from 133 clinically characterized, deceased individuals, including 75 infected with HIV. We developed a multimorbidity index based on the clinical disease history. Epigenetic age was moderately correlated across tissues. Blood had the greatest number and degree of correlation, most notably with spleen and bone marrow. However, blood did not correlate with epigenetic age of liver. EAA in liver was weakly correlated with EAA in kidney, adipose, lung and bone marrow. Clinically, hypertension was associated with EAA in several tissues, consistent with the multiorgan impacts of this illness. HIV infection was associated with positive age acceleration in kidney and spleen. Male sex was associated with increased epigenetic acceleration in several tissues. Preliminary evidence indicates that amyotrophic lateral sclerosis is associated with positive EAA in muscle tissue. Finally, greater multimorbidity was associated with greater EAA across all tissues. Blood alone will often fail to detect EAA in other tissues. While hypertension is associated with increased EAA in several tissues, many pathologies are associated with organ-specific age acceleration.

@article{masters_chronic_2022,
	title = {Chronic {HIV} {Infection} and {Aging}: {Application} of a {Geroscience}-{Guided} {Approach}},
	volume = {89},
	issn = {1525-4135},
	shorttitle = {Chronic {HIV} {Infection} and {Aging}},
	url = {https://journals.lww.com/10.1097/QAI.0000000000002858},
	doi = {10.1097/QAI.0000000000002858},
	language = {en},
	number = {S1},
	urldate = {2022-11-22},
	journal = {JAIDS Journal of Acquired Immune Deficiency Syndromes},
	author = {Masters, Mary C. and Landay, Alan L. and Robbins, Paul D. and Tchkonia, Tamar and Kirkland, James L. and Kuchel, George A. and Niedernhofer, Laura J. and Palella, Frank J.},
	month = feb,
	year = {2022},
	pages = {S34--S46},
}

@article{crane_hiv_2022,
	title = {{HIV}, {Aging}, and {Comorbidities} {Research} in {Clinical} {Cohorts}: 3 {Lessons} {Learned} {Using} {Examples} {From} the {CNICS} {Cohort}},
	volume = {89},
	issn = {1525-4135},
	shorttitle = {{HIV}, {Aging}, and {Comorbidities} {Research} in {Clinical} {Cohorts}},
	url = {https://journals.lww.com/10.1097/QAI.0000000000002836},
	doi = {10.1097/QAI.0000000000002836},
	language = {en},
	number = {S1},
	urldate = {2022-11-22},
	journal = {JAIDS Journal of Acquired Immune Deficiency Syndromes},
	author = {Crane, Heidi M. and Drumright, Lydia},
	month = feb,
	year = {2022},
	pages = {S10--S14},
}

@article{ibrahim_khalil_agespecific_2022,
	title = {Age‐specific burden of cervical cancer associated with {\textless}span style="font-variant:small-caps;"{\textgreater}{HIV}{\textless}/span{\textgreater} : {A} global analysis with a focus on {\textless}span style="font-variant:small-caps;"{\textgreater}sub‐{Saharan}{\textless}/span{\textgreater} {Africa}},
	volume = {150},
	issn = {0020-7136, 1097-0215},
	shorttitle = {Age‐specific burden of cervical cancer associated with {\textless}span style="font-variant},
	url = {https://onlinelibrary.wiley.com/doi/10.1002/ijc.33841},
	doi = {10.1002/ijc.33841},
	language = {en},
	number = {5},
	urldate = {2022-11-22},
	journal = {International Journal of Cancer},
	author = {Ibrahim Khalil, Ahmadaye and Mpunga, Tharcisse and Wei, Feixue and Baussano, Iacopo and Martel, Catherine and Bray, Freddie and Stelzle, Dominik and Dryden‐Peterson, Scott and Jaquet, Antoine and Horner, Marie‐Josèphe and Awolude, Olutosin A. and Trejo, Mario Jesus and Mudini, Washington and Soliman, Amr S. and Sengayi‐Muchengeti, Mazvita and Coghill, Anna E. and Aardt, Matthys C. and De Vuyst, Hugo and Hawes, Stephen E. and Broutet, Nathalie and Dalal, Shona and Clifford, Gary M.},
	month = mar,
	year = {2022},
	pages = {761--772},
}

@article{rodes_ageing_2022,
	title = {Ageing with {HIV}: {Challenges} and biomarkers},
	volume = {77},
	issn = {23523964},
	shorttitle = {Ageing with {HIV}},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S2352396422000809},
	doi = {10.1016/j.ebiom.2022.103896},
	language = {en},
	urldate = {2022-11-22},
	journal = {eBioMedicine},
	author = {Rodés, Berta and Cadiñanos, Julen and Esteban-Cantos, Andrés and Rodríguez-Centeno, Javier and Arribas, José Ramón},
	month = mar,
	year = {2022},
	pages = {103896},
}

@article{ruiz_surviving_2022,
	title = {From surviving to thriving: the current status of the behavioral, social, and psychological issues of aging with {HIV}},
	volume = {17},
	issn = {1746-630X, 1746-6318},
	shorttitle = {From surviving to thriving},
	url = {https://journals.lww.com/10.1097/COH.0000000000000725},
	doi = {10.1097/COH.0000000000000725},
	language = {en},
	number = {2},
	urldate = {2022-11-22},
	journal = {Current Opinion in HIV and AIDS},
	author = {Ruiz, Erik L. and Greene, Karah Y. and Galea, Jerome T. and Brown, Brandon},
	month = mar,
	year = {2022},
	pages = {55--64},
}

@article{chauvin_mechanisms_2022,
	title = {Mechanisms of immune aging in {HIV}},
	volume = {136},
	issn = {0143-5221, 1470-8736},
	url = {https://portlandpress.com/clinsci/article/136/1/61/230598/Mechanisms-of-immune-aging-in-HIV},
	doi = {10.1042/CS20210344},
	abstract = {Abstract 
            Massive CD4+ T-cell depletion as well as sustained immune activation and inflammation are hallmarks of Human Immunodeficiency Virus (HIV)-1 infection. In recent years, an emerging concept draws an intriguing parallel between HIV-1 infection and aging. Indeed, many of the alterations that affect innate and adaptive immune subsets in HIV-infected individuals are reminiscent of the process of immune aging, characteristic of old age. These changes, of which the presumed cause is the systemic immune activation established in patients, likely participate in the immuno-incompetence described with HIV progression. With the success of antiretroviral therapy (ART), HIV-seropositive patients can now live for many years despite chronic viral infection. However, acquired immunodeficiency syndrome (AIDS)-related opportunistic infections have given way to chronic diseases as the leading cause of death since HIV infection. Therefore, the comparison between HIV-1 infected patients and uninfected elderly individuals goes beyond the sole onset of immunosenescence and extends to the deterioration of several physiological functions related to inflammation and systemic aging. In light of this observation, it is interesting to understand the precise link between immune activation and aging in HIV-1 infection to figure out how to best care for people living with HIV (PLWH).},
	language = {en},
	number = {1},
	urldate = {2022-11-22},
	journal = {Clinical Science},
	author = {Chauvin, Manon and Sauce, Delphine},
	month = jan,
	year = {2022},
	pages = {61--80},
}

Abstract Massive CD4+ T-cell depletion as well as sustained immune activation and inflammation are hallmarks of Human Immunodeficiency Virus (HIV)-1 infection. In recent years, an emerging concept draws an intriguing parallel between HIV-1 infection and aging. Indeed, many of the alterations that affect innate and adaptive immune subsets in HIV-infected individuals are reminiscent of the process of immune aging, characteristic of old age. These changes, of which the presumed cause is the systemic immune activation established in patients, likely participate in the immuno-incompetence described with HIV progression. With the success of antiretroviral therapy (ART), HIV-seropositive patients can now live for many years despite chronic viral infection. However, acquired immunodeficiency syndrome (AIDS)-related opportunistic infections have given way to chronic diseases as the leading cause of death since HIV infection. Therefore, the comparison between HIV-1 infected patients and uninfected elderly individuals goes beyond the sole onset of immunosenescence and extends to the deterioration of several physiological functions related to inflammation and systemic aging. In light of this observation, it is interesting to understand the precise link between immune activation and aging in HIV-1 infection to figure out how to best care for people living with HIV (PLWH).

@article{weinstein_life_2022,
	title = {Life {Instability} {Associated} with {Lower} {ART} {Adherence} and {Other} {Poor} {HIV}-{Related} {Care} {Outcomes} in {Older} {Adults} with {HIV}},
	issn = {1070-5503, 1532-7558},
	url = {https://link.springer.com/10.1007/s12529-022-10095-5},
	doi = {10.1007/s12529-022-10095-5},
	language = {en},
	urldate = {2022-11-22},
	journal = {International Journal of Behavioral Medicine},
	author = {Weinstein, Elliott R. and Harkness, Audrey and Ironson, Gail and Shrader, Cho-Hee and Duncan, Dustin T. and Safren, Steven A.},
	month = may,
	year = {2022},
}

@article{lopez_angel_signatures_2021,
	title = {Signatures of immune dysfunction in {HIV} and {HCV} infection share features with chronic inflammation in aging and persist after viral reduction or elimination},
	volume = {118},
	issn = {0027-8424, 1091-6490},
	url = {http://www.pnas.org/lookup/doi/10.1073/pnas.2022928118},
	doi = {10.1073/pnas.2022928118},
	abstract = {Chronic inflammation is thought to be a major cause of morbidity and mortality in aging, but whether similar mechanisms underlie dysfunction in infection-associated chronic inflammation is unclear. Here, we profiled the immune proteome, and cellular composition and signaling states in a cohort of aging individuals versus a set of HIV patients on long-term antiretroviral therapy therapy or hepatitis C virus (HCV) patients before and after sofosbuvir treatment. We found shared alterations in aging-associated and infection-associated chronic inflammation including T cell memory inflation, up-regulation of intracellular signaling pathways of inflammation, and diminished sensitivity to cytokines in lymphocytes and myeloid cells. In the HIV cohort, these dysregulations were evident despite viral suppression for over 10 y. Viral clearance in the HCV cohort partially restored cellular sensitivity to interferon-α, but many immune system alterations persisted for at least 1 y posttreatment. Our findings indicate that in the HIV and HCV cohorts, a broad remodeling and degradation of the immune system can persist for a year or more, even after the removal or drastic reduction of the pathogen load and that this shares some features of chronic inflammation in aging.},
	language = {en},
	number = {14},
	urldate = {2021-10-08},
	journal = {Proceedings of the National Academy of Sciences},
	author = {Lopez Angel, Cesar J. and Pham, Edward A. and Du, Huixun and Vallania, Francesco and Fram, Benjamin J. and Perez, Kevin and Nguyen, Thai and Rosenberg-Hasson, Yael and Ahmed, Aijaz and Dekker, Cornelia L. and Grant, Philip M. and Khatri, Purvesh and Maecker, Holden T. and Glenn, Jeffrey S. and Davis, Mark M. and Furman, David},
	month = apr,
	year = {2021},
	pages = {e2022928118},
}

Chronic inflammation is thought to be a major cause of morbidity and mortality in aging, but whether similar mechanisms underlie dysfunction in infection-associated chronic inflammation is unclear. Here, we profiled the immune proteome, and cellular composition and signaling states in a cohort of aging individuals versus a set of HIV patients on long-term antiretroviral therapy therapy or hepatitis C virus (HCV) patients before and after sofosbuvir treatment. We found shared alterations in aging-associated and infection-associated chronic inflammation including T cell memory inflation, up-regulation of intracellular signaling pathways of inflammation, and diminished sensitivity to cytokines in lymphocytes and myeloid cells. In the HIV cohort, these dysregulations were evident despite viral suppression for over 10 y. Viral clearance in the HCV cohort partially restored cellular sensitivity to interferon-α, but many immune system alterations persisted for at least 1 y posttreatment. Our findings indicate that in the HIV and HCV cohorts, a broad remodeling and degradation of the immune system can persist for a year or more, even after the removal or drastic reduction of the pathogen load and that this shares some features of chronic inflammation in aging.

@article{pereira_evaluation_2021,
	title = {Evaluation of a {Clinic} {Dedicated} to {People} {Aging} with {HIV} at {Chelsea} and {Westminster} {Hospital}: {Results} of a 10-{Year} {Experience}},
	issn = {0889-2229, 1931-8405},
	shorttitle = {Evaluation of a {Clinic} {Dedicated} to {People} {Aging} with {HIV} at {Chelsea} and {Westminster} {Hospital}},
	url = {https://www.liebertpub.com/doi/10.1089/aid.2021.0083},
	doi = {10.1089/aid.2021.0083},
	language = {en},
	urldate = {2021-10-08},
	journal = {AIDS Research and Human Retroviruses},
	author = {Pereira, Branca and Mazzitelli, Maria and Milinkovic, Ana and Casley, Christina and Rubio, Javier and Channa, Rachel and Girometti, Nicolo and Asboe, David and Pozniak, Anton and Boffito, Marta},
	month = aug,
	year = {2021},
	pages = {aid.2021.0083},
}

@article{shiau_epigenetic_2021,
	title = {Epigenetic {Aging} {Biomarkers} {Associated} {With} {Cognitive} {Impairment} in {Older} {African} {American} {Adults} {With} {Human} {Immunodeficiency} {Virus} ({HIV})},
	issn = {1058-4838, 1537-6591},
	url = {https://academic.oup.com/cid/advance-article/doi/10.1093/cid/ciab563/6304900},
	doi = {10.1093/cid/ciab563},
	abstract = {Abstract 
             
              Background 
              Accelerated epigenetic aging using DNA methylation (DNAm)-based biomarkers has been reported in people with human immunodeficiency virus (HIV, PWH), but limited data are available among African Americans (AA), women, and older PWH. 
             
             
              Methods 
              DNAm was measured using Illumina EPIC Arrays for 107 (69 PWH and 38 HIV-seronegative controls) AA adults ≥60 years in New York City. Six DNAm-based biomarkers of aging were estimated: (1) epigenetic age acceleration (EAA), (2) extrinsic epigenetic age acceleration (EEAA), (3) intrinsic epigenetic age acceleration (IEAA), (4) GrimAge, (5) PhenoAge, and (6) DNAm-estimated telomere length (DNAm-TL). The National Institutes of Health (NIH) Toolbox Cognition Battery (domains: executive function, attention, working memory, processing speed, and language) and Montreal Cognitive Assessment (MoCA) were administered. Participants were assessed for frailty by the Fried criteria. 
             
             
              Results 
              The PWH and control groups did not differ by sex, chronological age, or ethnicity. In total, 83\% of PWH had a viral load \<50 copies/mL, and 94\% had a recent CD4 ≥200 cells/µL. The PWH group had a higher EAA, EEAA, GrimAge, and PhenoAge, and a lower DNAm-TL compared to the controls. IEAA was not different between groups. For PWH, there were significant negative correlations between IEAA and executive function, attention, and working memory and PhenoAge and attention. No associations between biomarkers and frailty were detected. 
             
             
              Conclusions 
              Evidence of epigenetic age acceleration was observed in AA older PWH using DNAm-based biomarkers of aging. There was no evidence of age acceleration independent of cell type National Institutes of Health composition (IEAA) associated with HIV, but this measure was associated with decreased cognitive function among PWH.},
	language = {en},
	urldate = {2021-10-08},
	journal = {Clinical Infectious Diseases},
	author = {Shiau, Stephanie and Arpadi, Stephen M and Shen, Yanhan and Cantos, Anyelina and Ramon, Christian Vivar and Shah, Jayesh and Jang, Grace and Manly, Jennifer J and Brickman, Adam M and Baccarelli, Andrea A and Yin, Michael T},
	month = jun,
	year = {2021},
	pages = {ciab563},
}

Abstract Background Accelerated epigenetic aging using DNA methylation (DNAm)-based biomarkers has been reported in people with human immunodeficiency virus (HIV, PWH), but limited data are available among African Americans (AA), women, and older PWH. Methods DNAm was measured using Illumina EPIC Arrays for 107 (69 PWH and 38 HIV-seronegative controls) AA adults ≥60 years in New York City. Six DNAm-based biomarkers of aging were estimated: (1) epigenetic age acceleration (EAA), (2) extrinsic epigenetic age acceleration (EEAA), (3) intrinsic epigenetic age acceleration (IEAA), (4) GrimAge, (5) PhenoAge, and (6) DNAm-estimated telomere length (DNAm-TL). The National Institutes of Health (NIH) Toolbox Cognition Battery (domains: executive function, attention, working memory, processing speed, and language) and Montreal Cognitive Assessment (MoCA) were administered. Participants were assessed for frailty by the Fried criteria. Results The PWH and control groups did not differ by sex, chronological age, or ethnicity. In total, 83% of PWH had a viral load <50 copies/mL, and 94% had a recent CD4 ≥200 cells/µL. The PWH group had a higher EAA, EEAA, GrimAge, and PhenoAge, and a lower DNAm-TL compared to the controls. IEAA was not different between groups. For PWH, there were significant negative correlations between IEAA and executive function, attention, and working memory and PhenoAge and attention. No associations between biomarkers and frailty were detected. Conclusions Evidence of epigenetic age acceleration was observed in AA older PWH using DNAm-based biomarkers of aging. There was no evidence of age acceleration independent of cell type National Institutes of Health composition (IEAA) associated with HIV, but this measure was associated with decreased cognitive function among PWH.

@article{schulz_prediction_2021,
	title = {Prediction of future cardiovascular events by {Framingham}, {SCORE} and {asCVD} risk scores is less accurate in {HIV}‐positive individuals from the {HIV}‐{HEART} {Study} compared with the general population},
	volume = {22},
	issn = {1464-2662, 1468-1293},
	url = {https://onlinelibrary.wiley.com/doi/10.1111/hiv.13124},
	doi = {10.1111/hiv.13124},
	language = {en},
	number = {8},
	urldate = {2021-10-08},
	journal = {HIV Medicine},
	author = {Schulz, C‐A and Mavarani, L and Reinsch, N and Albayrak‐Rena, S and Potthoff, A and Brockmeyer, N and Hower, M and Erbel, R and Jöckel, K‐H and Schmidt, B and Esser, S and {HIV HEART Aging Study Group and Heinz Nixdorf Recall Investigative Group}},
	month = sep,
	year = {2021},
	pages = {732--741},
}

@article{brennan-ing_aging_2021,
	title = {Aging {With} {HIV}: {Health} {Policy} and {Advocacy} {Priorities}},
	volume = {48},
	issn = {1090-1981, 1552-6127},
	shorttitle = {Aging {With} {HIV}},
	url = {http://journals.sagepub.com/doi/10.1177/1090198120984368},
	doi = {10.1177/1090198120984368},
	abstract = {The aging of people with HIV (PWH) is a major public health accomplishment and a social and cultural phenomenon. It highlights the human capacity to overcome adversity, the effectiveness of public health strategies (e.g., prevention and treatment), and the new challenges as well. Our societies are not well prepared to address the needs of older PWH and the changes they are creating. Stigma toward HIV, older age, and homosexuality, along with racism, have kept PWH largely invisible, resulting in limited investment in prevention and medical and social services. It is imperative that we develop an effective policy response to address the unique needs of PWH. The purpose of this article is to highlight current knowledge and emerging issues in HIV and aging to serve as a foundation on which to develop policy and program recommendations that will meet the new challenge.},
	language = {en},
	number = {1},
	urldate = {2021-10-08},
	journal = {Health Education \& Behavior},
	author = {Brennan-Ing, Mark and Ramirez-Valles, Jesus and Tax, Aaron},
	month = feb,
	year = {2021},
	pages = {5--8},
}

The aging of people with HIV (PWH) is a major public health accomplishment and a social and cultural phenomenon. It highlights the human capacity to overcome adversity, the effectiveness of public health strategies (e.g., prevention and treatment), and the new challenges as well. Our societies are not well prepared to address the needs of older PWH and the changes they are creating. Stigma toward HIV, older age, and homosexuality, along with racism, have kept PWH largely invisible, resulting in limited investment in prevention and medical and social services. It is imperative that we develop an effective policy response to address the unique needs of PWH. The purpose of this article is to highlight current knowledge and emerging issues in HIV and aging to serve as a foundation on which to develop policy and program recommendations that will meet the new challenge.

@article{aung_is_2021,
	title = {Is {There} {Any} {Evidence} of {Premature}, {Accentuated} and {Accelerated} {Aging} {Effects} on {Neurocognition} in {People} {Living} with {HIV}? {A} {Systematic} {Review}},
	volume = {25},
	issn = {1090-7165, 1573-3254},
	shorttitle = {Is {There} {Any} {Evidence} of {Premature}, {Accentuated} and {Accelerated} {Aging} {Effects} on {Neurocognition} in {People} {Living} with {HIV}?},
	url = {https://link.springer.com/10.1007/s10461-020-03053-3},
	doi = {10.1007/s10461-020-03053-3},
	abstract = {Abstract 
             
              Despite evidence of premature, accentuated and accelerated aging for some age-related conditions such as cardiovascular diseases in people living with HIV (PLHIV), the evidence for these abnormal patterns of aging on neurocognition remains unclear. Further, no systematic review has been dedicated to this issue. Using PRISMA guidelines, we searched standard databases (PubMed, EMBASE, CINAHL and PsycINFO). Articles were included if they analyzed and reported the effect of age on neurocognition among PLHIV as one of their major findings, if they were conducted in the combination anti-retroviral therapy era (after 1996) and published in a peer-reviewed journal in English. Quality appraisal was conducted using the Joanna Briggs Institute (JBI) appraisal tools. To systematically target the abnormal patterns of neurocognitive aging, we define 
              premature cognitive aging 
              as significant interaction effect of HIV status and age on cross-sectional neurocognitive test performance covering both the normal and abnormal performance range; 
              accentuated cognitive aging 
              as significant interaction effect of HIV status and age on cross-sectional neurocognitive impairment (NCI) rate, thus covering the abnormal performance range only; 
              accelerated cognitive aging 
              as significant interaction effect of HIV status and age on longitudinal neurocognitive test performance or incidence of NCI. Because these definitions require an age-comparable HIV-negative (HIV−) control group, when no controls were included, we determined the range of the age effect on neurocognitive test performance or NCI among PLHIV. A total of 37 studies originating from the US (26), UK (2), Italy (2), Poland (2), China (2), Japan (1), Australia (1), and Brazil (1) were included. Six studies were longitudinal and 14 included HIV- controls. The quality appraisal showed that 12/37 studies neither used an age-matched HIV- controls nor used demographically corrected cognitive scores. A meta-analysis was not possible because study methods and choice of neurocognitive measurement methods and outcomes were heterogeneous imposing a narrative synthesis. In studies with an HIV- control sample, premature neurocognitive aging was found in 45\% of the cross-sectional analyses (9/20), while accelerated neurocognitive aging was found in 75\% of the longitudinal analyses (3/4). There was no evidence for accentuated aging, but this was tested only in two studies. In studies without an HIV- control sample, the age effect was always present but wide (NCI OR = 1.18–4.8). While large sample size ({\textgreater} 500) was associated with abnormal patterns of cognitive aging, most of the studies were under powered. Other study characteristics such as longitudinal study design and higher proportion of older participants were also associated with the findings of abnormal cognitive aging. There is some support for premature and accelerated cognitive aging among PLHIV in the existing literature especially among large and longitudinal studies and those with higher proportion of older samples. Future HIV and cognitive aging studies need to harmonize neuropsychological measurement methods and outcomes and use a large sample from collaborative multi-sites to generate more robust evidences.},
	language = {en},
	number = {3},
	urldate = {2021-10-08},
	journal = {AIDS and Behavior},
	author = {Aung, Htein Linn and Aghvinian, Maral and Gouse, Hetta and Robbins, Reuben N. and Brew, Bruce J. and Mao, Limin and Cysique, Lucette A.},
	month = mar,
	year = {2021},
	pages = {917--960},
}

Abstract Despite evidence of premature, accentuated and accelerated aging for some age-related conditions such as cardiovascular diseases in people living with HIV (PLHIV), the evidence for these abnormal patterns of aging on neurocognition remains unclear. Further, no systematic review has been dedicated to this issue. Using PRISMA guidelines, we searched standard databases (PubMed, EMBASE, CINAHL and PsycINFO). Articles were included if they analyzed and reported the effect of age on neurocognition among PLHIV as one of their major findings, if they were conducted in the combination anti-retroviral therapy era (after 1996) and published in a peer-reviewed journal in English. Quality appraisal was conducted using the Joanna Briggs Institute (JBI) appraisal tools. To systematically target the abnormal patterns of neurocognitive aging, we define premature cognitive aging as significant interaction effect of HIV status and age on cross-sectional neurocognitive test performance covering both the normal and abnormal performance range; accentuated cognitive aging as significant interaction effect of HIV status and age on cross-sectional neurocognitive impairment (NCI) rate, thus covering the abnormal performance range only; accelerated cognitive aging as significant interaction effect of HIV status and age on longitudinal neurocognitive test performance or incidence of NCI. Because these definitions require an age-comparable HIV-negative (HIV−) control group, when no controls were included, we determined the range of the age effect on neurocognitive test performance or NCI among PLHIV. A total of 37 studies originating from the US (26), UK (2), Italy (2), Poland (2), China (2), Japan (1), Australia (1), and Brazil (1) were included. Six studies were longitudinal and 14 included HIV- controls. The quality appraisal showed that 12/37 studies neither used an age-matched HIV- controls nor used demographically corrected cognitive scores. A meta-analysis was not possible because study methods and choice of neurocognitive measurement methods and outcomes were heterogeneous imposing a narrative synthesis. In studies with an HIV- control sample, premature neurocognitive aging was found in 45% of the cross-sectional analyses (9/20), while accelerated neurocognitive aging was found in 75% of the longitudinal analyses (3/4). There was no evidence for accentuated aging, but this was tested only in two studies. In studies without an HIV- control sample, the age effect was always present but wide (NCI OR = 1.18–4.8). While large sample size (\textgreater 500) was associated with abnormal patterns of cognitive aging, most of the studies were under powered. Other study characteristics such as longitudinal study design and higher proportion of older participants were also associated with the findings of abnormal cognitive aging. There is some support for premature and accelerated cognitive aging among PLHIV in the existing literature especially among large and longitudinal studies and those with higher proportion of older samples. Future HIV and cognitive aging studies need to harmonize neuropsychological measurement methods and outcomes and use a large sample from collaborative multi-sites to generate more robust evidences.

@article{lew_reductions_2021,
	title = {Reductions in {Gray} {Matter} {Linked} to {Epigenetic} {HIV}-{Associated} {Accelerated} {Aging}},
	volume = {31},
	issn = {1047-3211, 1460-2199},
	url = {https://academic.oup.com/cercor/article/31/8/3752/6206851},
	doi = {10.1093/cercor/bhab045},
	abstract = {Abstract 
            A growing literature suggests a relationship between HIV-infection and a molecular profile of age acceleration. However, despite the widely known high prevalence of HIV-related brain atrophy and HIV-associated neurocognitive disorder (HAND), epigenetic age acceleration has not been linked to HIV-related changes in structural MRI. We applied morphological MRI methods to study the brain structure of 110 virally suppressed participants with HIV infection and 122 uninfected controls age 22–72. All participants were assessed for cognitive impairment, and blood samples were collected from a subset of 86 participants with HIV and 83 controls to estimate epigenetic age. We examined the group-level interactive effects of HIV and chronological age and then used individual estimations of epigenetic age to understand the relationship between age acceleration and brain structure. Finally, we studied the effects of HAND. HIV-infection was related to gray matter reductions, independent of age. However, using epigenetic age as a biomarker for age acceleration, individual HIV-related age acceleration was associated with reductions in total gray matter. HAND was associated with decreases in thalamic and hippocampal gray matter. In conclusion, despite viral suppression, accentuated gray matter loss is evident with HIV-infection, and greater biological age acceleration specifically relates to such gray matter loss.},
	language = {en},
	number = {8},
	urldate = {2021-10-08},
	journal = {Cerebral Cortex},
	author = {Lew, Brandon J and Schantell, Mikki D and O’Neill, Jennifer and Morsey, Brenda and Wang, Tina and Ideker, Trey and Swindells, Susan and Fox, Howard S and Wilson, Tony W},
	month = jul,
	year = {2021},
	pages = {3752--3763},
}

Abstract A growing literature suggests a relationship between HIV-infection and a molecular profile of age acceleration. However, despite the widely known high prevalence of HIV-related brain atrophy and HIV-associated neurocognitive disorder (HAND), epigenetic age acceleration has not been linked to HIV-related changes in structural MRI. We applied morphological MRI methods to study the brain structure of 110 virally suppressed participants with HIV infection and 122 uninfected controls age 22–72. All participants were assessed for cognitive impairment, and blood samples were collected from a subset of 86 participants with HIV and 83 controls to estimate epigenetic age. We examined the group-level interactive effects of HIV and chronological age and then used individual estimations of epigenetic age to understand the relationship between age acceleration and brain structure. Finally, we studied the effects of HAND. HIV-infection was related to gray matter reductions, independent of age. However, using epigenetic age as a biomarker for age acceleration, individual HIV-related age acceleration was associated with reductions in total gray matter. HAND was associated with decreases in thalamic and hippocampal gray matter. In conclusion, despite viral suppression, accentuated gray matter loss is evident with HIV-infection, and greater biological age acceleration specifically relates to such gray matter loss.

@article{arant_human_2021,
	title = {Human {Immunodeficiency} {Virus} ({HIV}) and {Aging}: {Multimorbidity} in {Older} {People} {With} {HIV} in {One} {Nonurban} {Southeastern} {Ryan} {White} {HIV}/{AIDS} {Program} {Clinic}},
	volume = {8},
	issn = {2328-8957},
	shorttitle = {Human {Immunodeficiency} {Virus} ({HIV}) and {Aging}},
	url = {https://academic.oup.com/ofid/article/doi/10.1093/ofid/ofaa584/6024520},
	doi = {10.1093/ofid/ofaa584},
	abstract = {Abstract 
             
              Background 
              Age-related chronic conditions are becoming more concerning for people with human immunodeficiency virus (PWH). We aimed to identify characteristics associated with multimorbidity and evaluate for association between multimorbidity and human immunodeficiency virus (HIV) outcomes. 
             
             
              Methods 
              Cohorts included PWH aged 45–89 with ≥1 medical visit at one Ryan White HIV/AIDS Program (RWHAP) Southeastern HIV clinic in 2006 (Cohort 1) or 2016 (Cohort 2). Multimorbidity was defined as ≥2 chronic diseases. We used multivariable logistic regression to assess for associations between characteristics and multimorbidity and between multimorbidity and HIV outcomes. 
             
             
              Results 
              Multimorbidity increased from Cohort 1 (n = 149) to Cohort 2 (n = 323) (18.8\% vs 29.7\%, P \< .001). Private insurance was associated with less multimorbidity than Medicare (Cohort 1: adjusted odds ratio [aOR] = 0.15, 95\% confidence interval [CI] = 0.02–0.63; Cohort 2: aOR = 0.53, 95\% CI = 0.27–1.00). In Cohort 2, multimorbidity was associated with female gender (aOR, 2.57; 95\% CI, 1.22–5.58). In Cohort 1, black participants were less likely to be engaged in care compared with non-black participants (aOR, 0.72; 95\% CI, 0.61–0.87). In Cohort 2, participants with rural residences were more likely to be engaged in care compared with those with urban residences (aOR, 1.23; 95\% CI, 1.10–1.38). Multimorbidity was not associated with differences in HIV outcomes. 
             
             
              Conclusions 
              Although PWH have access to RWHAP HIV care, PWH with private insurance had lower rates of multimorbidity, which may reflect better access to preventative non-HIV care. In 2016, multimorbidity was higher for women. The RWHAP and RWHAP Part D could invest in addressing these disparities related to insurance and gender.},
	language = {en},
	number = {1},
	urldate = {2021-10-08},
	journal = {Open Forum Infectious Diseases},
	author = {Arant, Elizabeth C and Harding, Ceshae and Geba, Maria and Targonski, Paul V and McManus, Kathleen A},
	month = jan,
	year = {2021},
	pages = {ofaa584},
}

Abstract Background Age-related chronic conditions are becoming more concerning for people with human immunodeficiency virus (PWH). We aimed to identify characteristics associated with multimorbidity and evaluate for association between multimorbidity and human immunodeficiency virus (HIV) outcomes. Methods Cohorts included PWH aged 45–89 with ≥1 medical visit at one Ryan White HIV/AIDS Program (RWHAP) Southeastern HIV clinic in 2006 (Cohort 1) or 2016 (Cohort 2). Multimorbidity was defined as ≥2 chronic diseases. We used multivariable logistic regression to assess for associations between characteristics and multimorbidity and between multimorbidity and HIV outcomes. Results Multimorbidity increased from Cohort 1 (n = 149) to Cohort 2 (n = 323) (18.8% vs 29.7%, P < .001). Private insurance was associated with less multimorbidity than Medicare (Cohort 1: adjusted odds ratio [aOR] = 0.15, 95% confidence interval [CI] = 0.02–0.63; Cohort 2: aOR = 0.53, 95% CI = 0.27–1.00). In Cohort 2, multimorbidity was associated with female gender (aOR, 2.57; 95% CI, 1.22–5.58). In Cohort 1, black participants were less likely to be engaged in care compared with non-black participants (aOR, 0.72; 95% CI, 0.61–0.87). In Cohort 2, participants with rural residences were more likely to be engaged in care compared with those with urban residences (aOR, 1.23; 95% CI, 1.10–1.38). Multimorbidity was not associated with differences in HIV outcomes. Conclusions Although PWH have access to RWHAP HIV care, PWH with private insurance had lower rates of multimorbidity, which may reflect better access to preventative non-HIV care. In 2016, multimorbidity was higher for women. The RWHAP and RWHAP Part D could invest in addressing these disparities related to insurance and gender.

@article{polanka_insomnia_2021,
	title = {Insomnia symptoms and biomarkers of monocyte activation, systemic inflammation, and coagulation in {HIV}: {Veterans} {Aging} {Cohort} {Study}},
	volume = {16},
	issn = {1932-6203},
	shorttitle = {Insomnia symptoms and biomarkers of monocyte activation, systemic inflammation, and coagulation in {HIV}},
	url = {https://dx.plos.org/10.1371/journal.pone.0246073},
	doi = {10.1371/journal.pone.0246073},
	abstract = {Background 
              Insomnia may be a risk factor for cardiovascular disease in HIV (HIV-CVD); however, mechanisms have yet to be elucidated. 
             
             
              Methods 
               
                We examined cross-sectional associations of insomnia symptoms with biological mechanisms of HIV-CVD (immune activation, systemic inflammation, and coagulation) among 1,542 people with HIV from the Veterans Aging Cohort Study (VACS) Biomarker Cohort. Past-month insomnia symptoms were assessed by the item, “Difficulty falling or staying asleep?,” with the following response options: “I do not have this symptom” or “I have this symptom and…” “it doesn’t bother me,” “it bothers me a little,” “it bothers me,” “it bothers me a lot.” Circulating levels of the monocyte activation marker soluble CD14 (sCD14), inflammatory marker interleukin-6 (IL-6), and coagulation marker D-dimer were determined from blood specimens. Demographic- and fully-adjusted (CVD risk factors, potential confounders, HIV-related factors) regression models were constructed, with log-transformed biomarker variables as the outcomes. We present the exponentiated regression coefficient (exp[b]) and its 95\% confidence interval ( 
                CI 
                ). 
               
             
             
              Results 
               
                We observed no significant associations between insomnia symptoms and sCD14 or IL-6. For D-dimer, veterans in the “Bothers a Lot” group had, on average, 17\% higher D-dimer than veterans in the “No Difficulty Falling or Staying Asleep” group in the demographic-adjusted model (exp[b] = 1.17, 95\% 
                CI 
                = 1.01–1.37, 
                p 
                = .04). This association was nonsignificant in the fully-adjusted model (exp[b] = 1.09, 95\% 
                CI 
                = 0.94–1.26, 
                p 
                = .27). 
               
             
             
              Conclusion 
              We observed little evidence of relationships between insomnia symptoms and markers of biological mechanisms of HIV-CVD. Other mechanisms may be responsible for the insomnia-CVD relationship in HIV; however, future studies with comprehensive assessments of insomnia symptoms are warranted.},
	language = {en},
	number = {2},
	urldate = {2021-10-08},
	journal = {PLOS ONE},
	author = {Polanka, Brittanny M. and Kundu, Suman and So-Armah, Kaku A. and Freiberg, Matthew S. and Gupta, Samir K. and Zapolski, Tamika C. B. and Hirsh, Adam T. and Bedimo, Roger J. and Budoff, Matthew J. and Butt, Adeel A. and Chang, Chung-Chou H. and Gottlieb, Stephen S. and Marconi, Vincent C. and Womack, Julie A. and Stewart, Jesse C.},
	editor = {Apetrei, Cristian},
	month = feb,
	year = {2021},
	pages = {e0246073},
}

Background Insomnia may be a risk factor for cardiovascular disease in HIV (HIV-CVD); however, mechanisms have yet to be elucidated. Methods We examined cross-sectional associations of insomnia symptoms with biological mechanisms of HIV-CVD (immune activation, systemic inflammation, and coagulation) among 1,542 people with HIV from the Veterans Aging Cohort Study (VACS) Biomarker Cohort. Past-month insomnia symptoms were assessed by the item, “Difficulty falling or staying asleep?,” with the following response options: “I do not have this symptom” or “I have this symptom and…” “it doesn’t bother me,” “it bothers me a little,” “it bothers me,” “it bothers me a lot.” Circulating levels of the monocyte activation marker soluble CD14 (sCD14), inflammatory marker interleukin-6 (IL-6), and coagulation marker D-dimer were determined from blood specimens. Demographic- and fully-adjusted (CVD risk factors, potential confounders, HIV-related factors) regression models were constructed, with log-transformed biomarker variables as the outcomes. We present the exponentiated regression coefficient (exp[b]) and its 95% confidence interval ( CI ). Results We observed no significant associations between insomnia symptoms and sCD14 or IL-6. For D-dimer, veterans in the “Bothers a Lot” group had, on average, 17% higher D-dimer than veterans in the “No Difficulty Falling or Staying Asleep” group in the demographic-adjusted model (exp[b] = 1.17, 95% CI = 1.01–1.37, p = .04). This association was nonsignificant in the fully-adjusted model (exp[b] = 1.09, 95% CI = 0.94–1.26, p = .27). Conclusion We observed little evidence of relationships between insomnia symptoms and markers of biological mechanisms of HIV-CVD. Other mechanisms may be responsible for the insomnia-CVD relationship in HIV; however, future studies with comprehensive assessments of insomnia symptoms are warranted.

@article{nguyen_hiv_2021,
	title = {“{HIV} and {Aging} in {Special} {Populations}: {From} the {Mitochondria} to the {Metropolis}”–{Proceedings} {From} the 2019 {Conference}},
	volume = {32},
	issn = {1055-3290, 1552-6917},
	shorttitle = {“{HIV} and {Aging} in {Special} {Populations}},
	url = {https://journals.lww.com/10.1097/JNC.0000000000000236},
	doi = {10.1097/JNC.0000000000000236},
	language = {en},
	number = {2},
	urldate = {2021-10-08},
	journal = {Journal of the Association of Nurses in AIDS Care},
	author = {Nguyen, Annie and Rinaldi, Stefano and Martinez, Claudia and Perkins, Molly and Holstad, Marcia McDonnell},
	month = mar,
	year = {2021},
	pages = {214--221},
}

@article{boldeanu_prevalence_2021,
	title = {Prevalence and {Characterization} of {Subclinical} {Coronary} {Atherosclerotic} {Plaque} with {CT} among {Individuals} with {HIV}: {Results} from the {Canadian} {HIV} and {Aging} {Cohort} {Study}},
	volume = {299},
	issn = {0033-8419, 1527-1315},
	shorttitle = {Prevalence and {Characterization} of {Subclinical} {Coronary} {Atherosclerotic} {Plaque} with {CT} among {Individuals} with {HIV}},
	url = {http://pubs.rsna.org/doi/10.1148/radiol.2021203297},
	doi = {10.1148/radiol.2021203297},
	language = {en},
	number = {3},
	urldate = {2021-10-08},
	journal = {Radiology},
	author = {Boldeanu, Irina and Sadouni, Manel and Mansour, Samer and Baril, Jean-Guy and Trottier, Benoît and Soulez, Gilles and S. Chin, Anne and Leipsic, Jonathon and Tremblay, Cécile and Durand, Madeleine and Chartrand-Lefebvre, Carl and {for the Canadian HIV and Aging Cohort Study Group} and Abrahamowicz, M. and Bernard, N. and Chomont, N. and Cloutier, G. and Conway, B. and Côté, J. and Dasilva, J. and El-Far, M. and Falutz, J. and Fortin, C. and Gaudreau, P. and Gill, M. J. and Harris, M. and Jenabian, M. A. and Juneau, D. and Monteith, K. and Lamarche, B. and Loutfy, M. and MacPherson, P. and Murray, M. and Pick, N. and Pilote, L. and Routy, J. P. and Margolese, S. and Thomas, R. and Trottier, S. and Tsoukas, C. and Walmsley, S. and Wong, A.},
	month = jun,
	year = {2021},
	pages = {571--580},
}

@article{lebrasseur_identifying_2021,
	title = {{IDENTIFYING} {BIOMARKERS} {FOR} {BIOLOGICAL} {AGE}: {GEROSCIENCE} {AND} {THE} {ICFSR} {TASK} {FORCE}},
	issn = {22734309},
	shorttitle = {{IDENTIFYING} {BIOMARKERS} {FOR} {BIOLOGICAL} {AGE}},
	url = {https://link.springer.com/article/10.14283/jfa.2021.5},
	doi = {10.14283/jfa.2021.5},
	abstract = {The International Conference on Frailty and Sarcopenia Research Task Force met in March 2020, in the shadow of the COVID-19 pandemic, to discuss strategies for advancing the interdisciplinary field of geroscience. Geroscience explores biological mechanisms of aging as targets for intervention that may delay the physiological consequences of aging, maintain function, and prevent frailty and disability. Priorities for clinical practice and research include identifying and validating a range of biomarkers of the hallmarks of aging. Potential biomarkers discussed included markers of mitochondrial dysfunction, proteostasis, stem cell dysfunction, nutrient sensing, genomic instability, telomere dysfunction, cellular senescence, and epigenetic changes. The FRAILOMICS initiative is exploring many of these through various omics studies. Translating this knowledge into new therapies is being addressed by the U.S. National Institute on Aging Translational Gerontology Branch. Research gaps identified by the Task Force include the need for improved cellular and animal models as well as more reliable and sensitive measures.},
	urldate = {2021-10-08},
	journal = {The Journal of Frailty \& Aging},
	author = {LeBrasseur, N.K. and de Cabo, R. and Fielding, R. and Ferrucci, L. and Rodriguez-Manas, L. and Viña, J. and Vellas, B.},
	year = {2021},
	pages = {1--6},
}

The International Conference on Frailty and Sarcopenia Research Task Force met in March 2020, in the shadow of the COVID-19 pandemic, to discuss strategies for advancing the interdisciplinary field of geroscience. Geroscience explores biological mechanisms of aging as targets for intervention that may delay the physiological consequences of aging, maintain function, and prevent frailty and disability. Priorities for clinical practice and research include identifying and validating a range of biomarkers of the hallmarks of aging. Potential biomarkers discussed included markers of mitochondrial dysfunction, proteostasis, stem cell dysfunction, nutrient sensing, genomic instability, telomere dysfunction, cellular senescence, and epigenetic changes. The FRAILOMICS initiative is exploring many of these through various omics studies. Translating this knowledge into new therapies is being addressed by the U.S. National Institute on Aging Translational Gerontology Branch. Research gaps identified by the Task Force include the need for improved cellular and animal models as well as more reliable and sensitive measures.

@article{derry_links_2021,
	title = {Links {Between} {Inflammation}, {Mood}, and {Physical} {Function} {Among} {Older} {Adults} {With} {HIV}},
	issn = {1079-5014, 1758-5368},
	url = {https://academic.oup.com/psychsocgerontology/advance-article/doi/10.1093/geronb/gbab027/6134450},
	doi = {10.1093/geronb/gbab027},
	abstract = {Abstract 
             
              Objectives 
              People living with human immunodeficiency virus (PLWH) treated with antiretrovirals have life spans similar to their HIV-negative peers. Yet, they experience elevated inflammation-related multimorbidity. Drawing on biopsychosocial determinants of health may inform interventions, but these links are understudied in older PLWH. We investigated cross-sectional relationships between psychosocial factors (mood, loneliness, and stigma), inflammatory markers, and age-related health outcomes among 143 PLWH aged 54–78 years. 
             
             
              Method 
              Participants provided blood samples for serum cytokine and C-reactive protein (CRP) analyses, completed surveys assessing psychosocial factors and health, and completed frailty assessments. Regression models tested relationships between key psychosocial-, inflammation, and age-related health variables, adjusting for relevant sociodemographic and clinical factors. 
             
             
              Results 
              Participants with more depressive symptoms had higher composite cytokine levels than those with fewer depressive symptoms (β = 0.22, t(126) = 2.71, p = .008). Those with higher cytokine levels were more likely to be prefrail or frail (adjusted odds ratio = 1.72, 95\% confidence interval = 1.01–2.93) and reported worse physical function (β = −0.23, t(129) = −2.64, p = .009) and more cognitive complaints (β = −0.20, t(129) = −2.16, p = .03) than those with lower cytokine levels. CRP was not significantly related to these outcomes; 6-month fall history was not significantly related to inflammatory markers. 
             
             
              Discussion 
              Novel approaches are needed to manage comorbidities and maximize quality of life among older PLWH. Illustrating key expected biopsychosocial links, our findings highlight several factors (e.g., depressive symptoms, poorer physical function) that may share bidirectional relationships with chronic inflammation, a key factor driving morbidity. These links may be leveraged to modify factors that drive excessive health risk among older PLWH.},
	language = {en},
	urldate = {2021-09-19},
	journal = {The Journals of Gerontology: Series B},
	author = {Derry, Heather M and Johnston, Carrie D and Burchett, Chelsie O and Brennan-Ing, Mark and Karpiak, Stephen and Zhu, Yuan-Shan and Siegler, Eugenia L and Glesby, Marshall J},
	editor = {Martire, Lynn},
	month = feb,
	year = {2021},
	pages = {gbab027},
}

Abstract Objectives People living with human immunodeficiency virus (PLWH) treated with antiretrovirals have life spans similar to their HIV-negative peers. Yet, they experience elevated inflammation-related multimorbidity. Drawing on biopsychosocial determinants of health may inform interventions, but these links are understudied in older PLWH. We investigated cross-sectional relationships between psychosocial factors (mood, loneliness, and stigma), inflammatory markers, and age-related health outcomes among 143 PLWH aged 54–78 years. Method Participants provided blood samples for serum cytokine and C-reactive protein (CRP) analyses, completed surveys assessing psychosocial factors and health, and completed frailty assessments. Regression models tested relationships between key psychosocial-, inflammation, and age-related health variables, adjusting for relevant sociodemographic and clinical factors. Results Participants with more depressive symptoms had higher composite cytokine levels than those with fewer depressive symptoms (β = 0.22, t(126) = 2.71, p = .008). Those with higher cytokine levels were more likely to be prefrail or frail (adjusted odds ratio = 1.72, 95% confidence interval = 1.01–2.93) and reported worse physical function (β = −0.23, t(129) = −2.64, p = .009) and more cognitive complaints (β = −0.20, t(129) = −2.16, p = .03) than those with lower cytokine levels. CRP was not significantly related to these outcomes; 6-month fall history was not significantly related to inflammatory markers. Discussion Novel approaches are needed to manage comorbidities and maximize quality of life among older PLWH. Illustrating key expected biopsychosocial links, our findings highlight several factors (e.g., depressive symptoms, poorer physical function) that may share bidirectional relationships with chronic inflammation, a key factor driving morbidity. These links may be leveraged to modify factors that drive excessive health risk among older PLWH.

@article{hileman_plasma_2021,
	title = {Plasma {Citrate} and {Succinate} {Are} {Associated} {With} {Neurocognitive} {Impairment} in {Older} {People} {With} {HIV}},
	volume = {73},
	issn = {1058-4838, 1537-6591},
	url = {https://academic.oup.com/cid/article/73/3/e765/6132094},
	doi = {10.1093/cid/ciab107},
	abstract = {Abstract 
             
              Background 
              Neurocognitive impairment (NCI) is associated with monocyte activation in people with HIV (PWH). Activated monocytes increase glycolysis, reduce oxidative phosphorylation, and accumulate citrate and succinate, tricarboxylic acid (TCA) cycle metabolites that promote inflammation—this metabolic shift may contribute to NCI and slowed gait speed in PWH. 
             
             
              Methods 
              Plasma citrate and succinate were assayed by liquid chromatography–mass spectrometry from 957 participants upon entry to a multicenter, prospective cohort of older PWH. Logistic, linear, and mixed-effects linear regression models were used to examine associations between entry/baseline TCA cycle metabolites and cross-sectional and longitudinal NCI, neuropsychological test scores (NPZ-4), and gait speed. 
             
             
              Results 
              Median age was 51 (range 40–78) years. Each 1 standard deviation (SD) citrate increment was associated with 1.18 higher odds of prevalent NCI at baseline (P = .03), 0.07 SD lower time-updated NPZ-4 score (P = .01), and 0.02 m/s slower time-updated gait speed (P \< .0001). Age accentuated these effects. In the oldest age-quartile, higher citrate was associated with 1.64 higher odds of prevalent NCI, 0.17 SD lower NPZ-4, and 0.04 m/s slower gait speed (P ≤ .01 for each). Similar associations were apparent with succinate in the oldest age-quintile, but not with gait speed. In participants without NCI at entry, higher citrate predicted a faster rate of neurocognitive decline. 
             
             
              Conclusions 
              Higher plasma citrate and succinate are associated with worse cross-sectional and longitudinal measures of neurocognitive function and gait speed that are age-dependent, supporting the importance of altered bioenergetic metabolism in the pathogenesis of NCI in older PWH.},
	language = {en},
	number = {3},
	urldate = {2021-09-19},
	journal = {Clinical Infectious Diseases},
	author = {Hileman, Corrilynn O and Kalayjian, Robert C and Azzam, Sausan and Schlatzer, Daniela and Wu, Kunling and Tassiopoulos, Katherine and Bedimo, Roger and Ellis, Ronald J and Erlandson, Kristine M and Kallianpur, Asha and Koletar, Susan L and Landay, Alan L and Palella, Frank J and Taiwo, Babafemi and Pallaki, Muralidhar and Hoppel, Charles L},
	month = aug,
	year = {2021},
	pages = {e765--e772},
}

Abstract Background Neurocognitive impairment (NCI) is associated with monocyte activation in people with HIV (PWH). Activated monocytes increase glycolysis, reduce oxidative phosphorylation, and accumulate citrate and succinate, tricarboxylic acid (TCA) cycle metabolites that promote inflammation—this metabolic shift may contribute to NCI and slowed gait speed in PWH. Methods Plasma citrate and succinate were assayed by liquid chromatography–mass spectrometry from 957 participants upon entry to a multicenter, prospective cohort of older PWH. Logistic, linear, and mixed-effects linear regression models were used to examine associations between entry/baseline TCA cycle metabolites and cross-sectional and longitudinal NCI, neuropsychological test scores (NPZ-4), and gait speed. Results Median age was 51 (range 40–78) years. Each 1 standard deviation (SD) citrate increment was associated with 1.18 higher odds of prevalent NCI at baseline (P = .03), 0.07 SD lower time-updated NPZ-4 score (P = .01), and 0.02 m/s slower time-updated gait speed (P < .0001). Age accentuated these effects. In the oldest age-quartile, higher citrate was associated with 1.64 higher odds of prevalent NCI, 0.17 SD lower NPZ-4, and 0.04 m/s slower gait speed (P ≤ .01 for each). Similar associations were apparent with succinate in the oldest age-quintile, but not with gait speed. In participants without NCI at entry, higher citrate predicted a faster rate of neurocognitive decline. Conclusions Higher plasma citrate and succinate are associated with worse cross-sectional and longitudinal measures of neurocognitive function and gait speed that are age-dependent, supporting the importance of altered bioenergetic metabolism in the pathogenesis of NCI in older PWH.

@article{masters_baseline_2021,
	title = {Baseline {Neurocognitive} {Impairment} ({NCI}) {Is} {Associated} {With} {Incident} {Frailty} but {Baseline} {Frailty} {Does} {Not} {Predict} {Incident} {NCI} in {Older} {Persons} {With} {Human} {Immunodeficiency} {Virus} ({HIV})},
	volume = {73},
	issn = {1058-4838, 1537-6591},
	url = {https://academic.oup.com/cid/article/73/4/680/6134303},
	doi = {10.1093/cid/ciab122},
	abstract = {Abstract 
             
              Background 
              Neurocognitive impairment (NCI) and frailty are more prevalent among persons with human immunodeficiency virus (HIV, PWH) compared to those without HIV. Frailty and NCI often overlap with one another. Whether frailty precedes declines in neurocognitive function among PWH or vice versa has not been well established. 
             
             
              Methods 
              AIDS Clinical Trials Group (ACTG) A5322 is an observational cohort study of older PWH. Participants undergo annual assessments for NCI and frailty. ACTG A5322 participants who developed NCI as indexed by tests of impaired executive functioning and processing speed during the first 3 years were compared to persons who maintained normal cognitive function; those who demonstrated resolution of NCI were compared to those who had persistent NCI. Participants were similarly compared by frailty trajectory. We fit multinomial logistic regression models to assess associations between baseline covariates (including NCI) and frailty, and associations between baseline covariates (including frailty) and NCI. 
             
             
              Results 
              In total, 929 participants were included with a median age of 51 years (interquartile range [IQR] 46–56). At study entry, 16\% had NCI, and 6\% were frail. Over 3 years, 6\% of participants developed NCI; 5\% developed frailty. NCI was associated with development of frailty (odds ratio [OR] = 2.06; 95\% confidence interval [CI] = .94, 4.48; P = .07). Further adjustment for confounding strengthened this association (OR = 2.79; 95\% CI = 1.21, 6.43; P = .02). Baseline frailty however was not associated with NCI development. 
             
             
              Conclusions 
              NCI was associated with increased risk of frailty, but frailty was not associated with development of NCI. These findings suggest that the presence of NCI in PWH should prompt monitoring for the development of frailty and interventions to prevent frailty in this population.},
	language = {en},
	number = {4},
	urldate = {2021-09-19},
	journal = {Clinical Infectious Diseases},
	author = {Masters, Mary Clare and Perez, Jeremiah and Wu, Kunling and Ellis, Ronald J and Goodkin, Karl and Koletar, Susan L and Andrade, Adriana and Yang, Jingyan and Brown, Todd T and Palella, Frank J and Sacktor, Ned and Tassiopoulos, Katherine and Erlandson, Kristine M},
	month = aug,
	year = {2021},
	pages = {680--688},
}

Abstract Background Neurocognitive impairment (NCI) and frailty are more prevalent among persons with human immunodeficiency virus (HIV, PWH) compared to those without HIV. Frailty and NCI often overlap with one another. Whether frailty precedes declines in neurocognitive function among PWH or vice versa has not been well established. Methods AIDS Clinical Trials Group (ACTG) A5322 is an observational cohort study of older PWH. Participants undergo annual assessments for NCI and frailty. ACTG A5322 participants who developed NCI as indexed by tests of impaired executive functioning and processing speed during the first 3 years were compared to persons who maintained normal cognitive function; those who demonstrated resolution of NCI were compared to those who had persistent NCI. Participants were similarly compared by frailty trajectory. We fit multinomial logistic regression models to assess associations between baseline covariates (including NCI) and frailty, and associations between baseline covariates (including frailty) and NCI. Results In total, 929 participants were included with a median age of 51 years (interquartile range [IQR] 46–56). At study entry, 16% had NCI, and 6% were frail. Over 3 years, 6% of participants developed NCI; 5% developed frailty. NCI was associated with development of frailty (odds ratio [OR] = 2.06; 95% confidence interval [CI] = .94, 4.48; P = .07). Further adjustment for confounding strengthened this association (OR = 2.79; 95% CI = 1.21, 6.43; P = .02). Baseline frailty however was not associated with NCI development. Conclusions NCI was associated with increased risk of frailty, but frailty was not associated with development of NCI. These findings suggest that the presence of NCI in PWH should prompt monitoring for the development of frailty and interventions to prevent frailty in this population.

@article{weinstein_hivaids_2021,
	title = {{HIV}/{AIDS} and aging: the new frontier for {HIV}/{AIDS} research and care},
	volume = {35},
	issn = {0269-9370, 1473-5571},
	shorttitle = {{HIV}/{AIDS} and aging},
	url = {https://journals.lww.com/10.1097/QAD.0000000000003000},
	doi = {10.1097/QAD.0000000000003000},
	language = {en},
	number = {12},
	urldate = {2021-09-19},
	journal = {AIDS},
	author = {Weinstein, Elliott R. and Lee, Jasper S. and Mendez, Noelle A. and Harkness, Audrey and Safren, Steven A. and El-Sadr, Wafaa},
	month = oct,
	year = {2021},
	pages = {2043--2045},
}

@article{crane_brief_2021,
	title = {Brief {Report}: {Differences} in {Types} of {Myocardial} {Infarctions} {Among} {People} {Aging} {With} {HIV}},
	volume = {86},
	issn = {1525-4135},
	shorttitle = {Brief {Report}},
	url = {https://journals.lww.com/10.1097/QAI.0000000000002534},
	doi = {10.1097/QAI.0000000000002534},
	language = {en},
	number = {2},
	urldate = {2021-04-22},
	journal = {JAIDS Journal of Acquired Immune Deficiency Syndromes},
	author = {Crane, Heidi M. and Nance, Robin M. and Whitney, Bridget M. and Heckbert, Susan R. and Budoff, Matthew and High, Kevin and Landay, Alan and Feinstein, Matthew and Moore, Richard D. and Mathews, William Christopher and Christopoulos, Katerina and Saag, Michael S. and Willig, Amanda and Eron, Joseph J. and Kitahata, Mari M. and Delaney, Joseph A. C. and {for the Centers for AIDS Research Network of Clinical Information Systems}},
	month = feb,
	year = {2021},
	pages = {208--212},
}

@article{j_lew_reductions_2021,
	title = {Reductions in {Gray} {Matter} {Linked} to {Epigenetic} {HIV}-{Associated} {Accelerated} {Aging}},
	issn = {1047-3211, 1460-2199},
	url = {https://academic.oup.com/cercor/advance-article/doi/10.1093/cercor/bhab045/6206851},
	doi = {10.1093/cercor/bhab045},
	abstract = {Abstract 
            A growing literature suggests a relationship between HIV-infection and a molecular profile of age acceleration. However, despite the widely known high prevalence of HIV-related brain atrophy and HIV-associated neurocognitive disorder (HAND), epigenetic age acceleration has not been linked to HIV-related changes in structural MRI. We applied morphological MRI methods to study the brain structure of 110 virally suppressed participants with HIV infection and 122 uninfected controls age 22–72. All participants were assessed for cognitive impairment, and blood samples were collected from a subset of 86 participants with HIV and 83 controls to estimate epigenetic age. We examined the group-level interactive effects of HIV and chronological age and then used individual estimations of epigenetic age to understand the relationship between age acceleration and brain structure. Finally, we studied the effects of HAND. HIV-infection was related to gray matter reductions, independent of age. However, using epigenetic age as a biomarker for age acceleration, individual HIV-related age acceleration was associated with reductions in total gray matter. HAND was associated with decreases in thalamic and hippocampal gray matter. In conclusion, despite viral suppression, accentuated gray matter loss is evident with HIV-infection, and greater biological age acceleration specifically relates to such gray matter loss.},
	language = {en},
	urldate = {2021-04-22},
	journal = {Cerebral Cortex},
	author = {J Lew, Brandon and Schantell, Mikki D and O’Neill, Jennifer and Morsey, Brenda and Wang, Tina and Ideker, Trey and Swindells, Susan and S Fox, Howard and Wilson, Tony W},
	month = apr,
	year = {2021},
	pages = {bhab045},
}

Abstract A growing literature suggests a relationship between HIV-infection and a molecular profile of age acceleration. However, despite the widely known high prevalence of HIV-related brain atrophy and HIV-associated neurocognitive disorder (HAND), epigenetic age acceleration has not been linked to HIV-related changes in structural MRI. We applied morphological MRI methods to study the brain structure of 110 virally suppressed participants with HIV infection and 122 uninfected controls age 22–72. All participants were assessed for cognitive impairment, and blood samples were collected from a subset of 86 participants with HIV and 83 controls to estimate epigenetic age. We examined the group-level interactive effects of HIV and chronological age and then used individual estimations of epigenetic age to understand the relationship between age acceleration and brain structure. Finally, we studied the effects of HAND. HIV-infection was related to gray matter reductions, independent of age. However, using epigenetic age as a biomarker for age acceleration, individual HIV-related age acceleration was associated with reductions in total gray matter. HAND was associated with decreases in thalamic and hippocampal gray matter. In conclusion, despite viral suppression, accentuated gray matter loss is evident with HIV-infection, and greater biological age acceleration specifically relates to such gray matter loss.

@article{pahwa_nih_2021,
	title = {{NIH} {Workshop} on {HIV}-{Associated} {Comorbidities}, {Coinfections}, and {Complications}: {Summary} and {Recommendation} for {Future} {Research}},
	volume = {86},
	issn = {1525-4135},
	shorttitle = {{NIH} {Workshop} on {HIV}-{Associated} {Comorbidities}, {Coinfections}, and {Complications}},
	url = {https://journals.lww.com/jaids/Abstract/2021/01010/NIH_Workshop_on_HIV_Associated_Comorbidities,.2.aspx},
	doi = {10.1097/QAI.0000000000002528},
	abstract = {Background: 
        With potent antiretroviral therapy and simplified regimens, people living with HIV (PWH) are achieving near-normal lifespans but not necessarily a normal health span or healthy aging. PWH have a higher than expected risk of developing a number of non-AIDS comorbidities, coinfections, and complications (CCC), often against a background of stigma, poverty, and isolation.
        Setting: 
        To gain a better understanding of research needs for HIV-associated CCC, the NIH convened a 2-day workshop (HIV-associated CCC, or HIV ACTION).
        Methods: 
        A cross-institute NIH planning committee identified 6 key research areas: epidemiology and population research, pathogenesis and basic science research, clinical research, implementation science research, syndemics research and international research in low and middle income countries. Investigators were selected to lead working groups (WGs) to assess the state-of-the-art and identify 3–5 priority areas in each field before the workshop. A 2-day program at the NIH was developed which included presentations by invited experts and WG members.
        Results: 
        Over 400 participants attended the workshop. After general and individual WG discussions, the most pressing gaps, questions, or proposed action items were identified. Priority lists of pressing research issues were presented by cochairs of each WG. A detailed report is posted at the NHLBI website. This article reports the streamlined priority list and a summary of WG discussions to inform investigators of current priorities in the field.
        Conclusion: 
        Collaborative efforts of many disciplines are needed to improve the health and wellbeing of PWH. Several common themes emerged across WG representing potential priorities for investigators and recommendations for the NIH.},
	language = {en-US},
	number = {1},
	urldate = {2020-12-21},
	journal = {JAIDS Journal of Acquired Immune Deficiency Syndromes},
	author = {Pahwa, Savita and Deeks, Steven and Zou, Shimian and Tomitch, Natalie and Miller-Novak, Leia and Caler, Elisabet and Justice, Amy and Sacktor, Ned and Gabuzda, Dana and Hunt, Peter W. and Brown, Todd and Kurth, Ann and Baral, Stefan and Mugavero, Michael and Mayer, Kenneth H. and Mendenhall, Emily and Detels, Roger and Mutabazi, Vincent},
	month = jan,
	year = {2021},
	pages = {11--18},
}

Background:  With potent antiretroviral therapy and simplified regimens, people living with HIV (PWH) are achieving near-normal lifespans but not necessarily a normal health span or healthy aging. PWH have a higher than expected risk of developing a number of non-AIDS comorbidities, coinfections, and complications (CCC), often against a background of stigma, poverty, and isolation. Setting:  To gain a better understanding of research needs for HIV-associated CCC, the NIH convened a 2-day workshop (HIV-associated CCC, or HIV ACTION). Methods:  A cross-institute NIH planning committee identified 6 key research areas: epidemiology and population research, pathogenesis and basic science research, clinical research, implementation science research, syndemics research and international research in low and middle income countries. Investigators were selected to lead working groups (WGs) to assess the state-of-the-art and identify 3–5 priority areas in each field before the workshop. A 2-day program at the NIH was developed which included presentations by invited experts and WG members. Results:  Over 400 participants attended the workshop. After general and individual WG discussions, the most pressing gaps, questions, or proposed action items were identified. Priority lists of pressing research issues were presented by cochairs of each WG. A detailed report is posted at the NHLBI website. This article reports the streamlined priority list and a summary of WG discussions to inform investigators of current priorities in the field. Conclusion:  Collaborative efforts of many disciplines are needed to improve the health and wellbeing of PWH. Several common themes emerged across WG representing potential priorities for investigators and recommendations for the NIH.

@article{lake_risk_2020,
	title = {Risk {Factors} for {Weight} {Gain} {Following} {Switch} to {Integrase} {Inhibitor}–{Based} {Antiretroviral} {Therapy}},
	volume = {71},
	issn = {1058-4838, 1537-6591},
	url = {https://academic.oup.com/cid/article/71/9/e471/5758067},
	doi = {10.1093/cid/ciaa177},
	abstract = {Abstract 
             
              Background 
              Treatment initiation with integrase strand transfer inhibitors (INSTIs) has been associated with excess weight gain. Whether similar gains are seen after switch to INSTIs among virologically suppressed persons is less clear. We assessed pre/post-INSTI weight changes from AIDS Clinical Trials Group participants (A5001 and A5322). 
             
             
              Methods 
              Participants who were in follow-up from 1997–2017 and switched to INSTI-based antiretroviral regimens were included. Piecewise linear mixed-effects models adjusting for age, sex, race/ethnicity, baseline BMI, nadir and current CD4+ T-cell count, smoking, diabetes and follow-up time with suppressed HIV-1 RNA examined weight and waist circumference change before and after first switch to INSTIs. Linear spline models with a single knot at time of switch accounted for nonlinear trends. 
             
             
              Results 
              The 972 participants who switched to INSTIs were 81\% male and 50\% nonwhite with a median age at switch of 50 years, CD4+ T-cell count 512 cells/μL, and BMI 26.4 kg/m2. Restricting to persons with suppressed HIV-1 RNA at switch (n = 691), women, blacks, and persons ≥60 years experienced greater weight gain in the 2 years after versus before switch. In adjusted models, white or black race, age ≥60, and BMI ≥30 kg/m2 at switch were associated with greater weight gain following switch among women; age ≥60 was the greatest risk factor among men. Trends for waist circumference were similar. 
             
             
              Conclusions 
              Yearly weight gain increased following switch to INSTIs, particularly for women, blacks, and persons aged ≥60. Concomitant increases in waist circumference suggest that this weight gain is associated with an increase in fat mass.},
	language = {en},
	number = {9},
	urldate = {2021-09-19},
	journal = {Clinical Infectious Diseases},
	author = {Lake, Jordan E and Wu, Kunling and Bares, Sara H and Debroy, Paula and Godfrey, Catherine and Koethe, John R and McComsey, Grace A and Palella, Frank J and Tassiopoulos, Katherine and Erlandson, Kristine M},
	month = dec,
	year = {2020},
	pages = {e471--e477},
}

Abstract Background Treatment initiation with integrase strand transfer inhibitors (INSTIs) has been associated with excess weight gain. Whether similar gains are seen after switch to INSTIs among virologically suppressed persons is less clear. We assessed pre/post-INSTI weight changes from AIDS Clinical Trials Group participants (A5001 and A5322). Methods Participants who were in follow-up from 1997–2017 and switched to INSTI-based antiretroviral regimens were included. Piecewise linear mixed-effects models adjusting for age, sex, race/ethnicity, baseline BMI, nadir and current CD4+ T-cell count, smoking, diabetes and follow-up time with suppressed HIV-1 RNA examined weight and waist circumference change before and after first switch to INSTIs. Linear spline models with a single knot at time of switch accounted for nonlinear trends. Results The 972 participants who switched to INSTIs were 81% male and 50% nonwhite with a median age at switch of 50 years, CD4+ T-cell count 512 cells/μL, and BMI 26.4 kg/m2. Restricting to persons with suppressed HIV-1 RNA at switch (n = 691), women, blacks, and persons ≥60 years experienced greater weight gain in the 2 years after versus before switch. In adjusted models, white or black race, age ≥60, and BMI ≥30 kg/m2 at switch were associated with greater weight gain following switch among women; age ≥60 was the greatest risk factor among men. Trends for waist circumference were similar. Conclusions Yearly weight gain increased following switch to INSTIs, particularly for women, blacks, and persons aged ≥60. Concomitant increases in waist circumference suggest that this weight gain is associated with an increase in fat mass.

@article{de_francesco_multimorbidity_2020,
	title = {Multimorbidity patterns in people with {HIV}:},
	volume = {15},
	issn = {1746-630X},
	shorttitle = {Multimorbidity patterns in people with {HIV}},
	url = {http://journals.lww.com/10.1097/COH.0000000000000595},
	doi = {10.1097/COH.0000000000000595},
	language = {en},
	number = {2},
	urldate = {2021-04-22},
	journal = {Current Opinion in HIV and AIDS},
	author = {De Francesco, Davide and Sabin, Caroline A. and Reiss, Peter},
	month = mar,
	year = {2020},
	pages = {110--117},
}

@article{hunt_mitochondria_2020,
	title = {Mitochondria and ageing with {HIV}:},
	volume = {15},
	issn = {1746-630X},
	shorttitle = {Mitochondria and ageing with {HIV}},
	url = {http://journals.lww.com/10.1097/COH.0000000000000607},
	doi = {10.1097/COH.0000000000000607},
	language = {en},
	number = {2},
	urldate = {2021-04-22},
	journal = {Current Opinion in HIV and AIDS},
	author = {Hunt, Matthew and Payne, Brendan A.I.},
	month = mar,
	year = {2020},
	pages = {101--109},
}

@article{szaniawski_senotherapeutics_2020,
	title = {Senotherapeutics for {HIV} and aging:},
	volume = {15},
	issn = {1746-630X},
	shorttitle = {Senotherapeutics for {HIV} and aging},
	url = {http://journals.lww.com/10.1097/COH.0000000000000609},
	doi = {10.1097/COH.0000000000000609},
	language = {en},
	number = {2},
	urldate = {2021-04-22},
	journal = {Current Opinion in HIV and AIDS},
	author = {Szaniawski, Matthew A. and Spivak, Adam M.},
	month = mar,
	year = {2020},
	pages = {83--93},
}

@article{bygrave_lets_2020,
	title = {Let's talk chronic disease: can differentiated service delivery address the syndemics of {HIV}, hypertension and diabetes?},
	volume = {Publish Ahead of Print},
	issn = {1746-630X},
	shorttitle = {Let's talk chronic disease},
	url = {https://journals.lww.com/10.1097/COH.0000000000000629},
	doi = {10.1097/COH.0000000000000629},
	language = {en},
	urldate = {2021-04-22},
	journal = {Current Opinion in HIV and AIDS},
	author = {Bygrave, Helen and Golob, Lina and Wilkinson, Lynne and Roberts, Teri and Grimsrud, Anna},
	month = may,
	year = {2020},
}

@article{womack_oath_2020,
	title = {The {OATH} {Syndemic}: opioids and other substances, aging, alcohol, tobacco, and {HIV}},
	volume = {Publish Ahead of Print},
	issn = {1746-630X},
	shorttitle = {The {OATH} {Syndemic}},
	url = {https://journals.lww.com/10.1097/COH.0000000000000635},
	doi = {10.1097/COH.0000000000000635},
	language = {en},
	urldate = {2021-04-22},
	journal = {Current Opinion in HIV and AIDS},
	author = {Womack, Julie A. and Justice, Amy C.},
	month = jun,
	year = {2020},
}

@article{piggott_frailty_2020,
	title = {Frailty transitions, inflammation, and mortality among persons aging with {HIV} infection and injection drug use},
	volume = {34},
	issn = {0269-9370, 1473-5571},
	url = {https://journals.lww.com/10.1097/QAD.0000000000002527},
	doi = {10.1097/QAD.0000000000002527},
	language = {en},
	number = {8},
	urldate = {2020-12-16},
	journal = {AIDS},
	author = {Piggott, Damani A. and Bandeen-Roche, Karen and Mehta, Shruti H. and Brown, Todd T. and Yang, Huanle and Walston, Jeremy D. and Leng, Sean X. and Kirk, Gregory D.},
	month = jul,
	year = {2020},
	pages = {1217--1225},
}

@article{rowell-cunsolo_trends_2020,
	title = {Trends in comorbidities among {HIV}-infected hospital admissions in {New} {York} {City} from 2006-2016},
	url = {https://academic.oup.com/cid/advance-article/doi/10.1093/cid/ciaa1760/6007542},
	doi = {10.1093/cid/ciaa1760},
	abstract = {AbstractBackground. Due to the advent and success of antiretroviral therapy (ART), the number of people living and aging with HIV has grown substantially. Altho},
	language = {en},
	urldate = {2020-12-04},
	journal = {Clinical Infectious Diseases},
	author = {Rowell-Cunsolo, Tawandra L. and Hu, Gloria and Bellerose, Meghan and Liu, Jianfang},
	year = {2020},
}

AbstractBackground. Due to the advent and success of antiretroviral therapy (ART), the number of people living and aging with HIV has grown substantially. Altho

@article{peters_food_2020,
	title = {Food insecurity and {T}-cell dysregulation in women living with {HIV} on antiretroviral therapy},
	url = {https://academic.oup.com/cid/advance-article/doi/10.1093/cid/ciaa1771/6009049},
	doi = {10.1093/cid/ciaa1771},
	abstract = {AbstractBackground. Food insecurity is associated with increased morbidity and mortality in people living with HIV on antiretroviral therapy, but its relationsh},
	language = {en},
	urldate = {2020-12-04},
	journal = {Clinical Infectious Diseases},
	author = {Peters, Brandilyn A. and Sheira, Lila A. and Hanna, David B. and Qi, Qibin and Sharma, Anjali and Adedimeji, Adebola and Wilson, Tracey and Merenstein, Daniel and Tien, Phyllis C. and Cohen, Mardge and Wentz, Eryka L. and Kinslow, Jennifer and Landay, Alan L. and Weiser, Sheri D.},
	year = {2020},
}

AbstractBackground. Food insecurity is associated with increased morbidity and mortality in people living with HIV on antiretroviral therapy, but its relationsh

@article{abdo_associations_2020,
	title = {Associations between {Tenofovir} {Diphosphate} in {Dried} {Blood} {Spots}, {Impaired} {Physical} {Function}, and {Fracture} {Risk}},
	url = {https://academic.oup.com/ofid/advance-article/doi/10.1093/ofid/ofaa577/6007508},
	doi = {10.1093/ofid/ofaa577},
	abstract = {AbstractObjective. Evaluate associations between cumulative antiretroviral adherence/exposure, quantified using tenofovir diphosphate (TFV-DP) in dried blood sp},
	language = {en},
	urldate = {2020-12-04},
	journal = {Open Forum Infectious Diseases},
	author = {Abdo, Mona and Coyle, Ryan P. and Seifert, Sharon M. and Castillo-Mancilla, Jose R. and Jankowski, Catherine M. and MaWhinney, Samantha and Anderson, Peter L. and Erlandson, Kristine M.},
	year = {2020},
}

AbstractObjective. Evaluate associations between cumulative antiretroviral adherence/exposure, quantified using tenofovir diphosphate (TFV-DP) in dried blood sp

@article{willig_physical_2020,
	title = {Physical activity trends and metabolic health outcomes in people living with {HIV} in the {US}, 2008–2015},
	volume = {63},
	issn = {00330620},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S0033062020300359},
	doi = {10.1016/j.pcad.2020.02.005},
	language = {en},
	number = {2},
	urldate = {2020-11-18},
	journal = {Progress in Cardiovascular Diseases},
	author = {Willig, Amanda L. and Webel, Allison R. and Westfall, Andrew O. and Levitan, Emily B. and Crane, Heidi M. and Buford, Thomas W. and Burkholder, Greer A. and Willig, James H. and Blashill, Aaron J. and Moore, Richard D. and Mathews, W. Christopher and Zinski, Anne and Muhammad, Josh and Geng, Elvin H. and Napravnik, Sonia and Eron, Joseph J. and Rodriguez, Benigno and Bamman, Marcas M. and Overton, E. Turner},
	month = mar,
	year = {2020},
	pages = {170--177},
}

@article{sehl_effects_2020,
	title = {The {Effects} of {Anti}-retroviral {Therapy} on {Epigenetic} {Age} {Acceleration} {Observed} in {HIV}-1-infected {Adults}},
	volume = {5},
	issn = {2469-2964},
	url = {https://paijournal.com/index.php/paijournal/article/view/376},
	doi = {10.20411/pai.v5i1.376},
	abstract = {Background: HIV-1 infection is associated with acceleration of age-related methylation patterns in peripheral blood and brain of infected individuals although the relative contributions of HIV-1 infection versus its treatment to the observed accelerations in biological aging have not yet been investigated. Methods: In this longitudinal study of the effects of antiretroviral therapy (ART) on epigenetic aging patterns, we extracted DNA from peripheral blood mononuclear cells from 15 HIV-1-infected individuals infected at three time points: 6 months-1year pre-ART, 6-12 months post-initiation of ART, and 18-24 months after initiating ART. We compared these trajectories with those of 15 age-matched uninfected control participants at three time points with similar intervals. Methylation studies were performed using the Infinium methylation 450 arrays. We examined four epigenetic clock measurements: Age acceleration residual (AAR), Extrinsic (EEAA), Phenotypic (PEAA), and Grim (GEAA) epigenetic age acceleration. Weighted correlation network (WGCNA) analysis was used to identify clusters of highly co-methylated CpGs. Results: We found that prior to the initiation of ART all four epigenetic measures were significantly higher in HIV-1-infected individuals compared with uninfected individuals (P{\textless}0.001 for AAR, P=0.008 for EEAA, P=0.012 for GEAA, P{\textless}0.001 for PEAA using Wilcoxon rank sum tests between serostatus groups). These effects persisted after the initiation of ART, although the magnitude of these differences diminished. At 18-24 months post-ART initiation (time point 3), PEAA and GEAA were no longer significantly different between HIV-1-infected and uninfected individuals (P=0.059 for PEAA, P=0.11 for GEAA), while AAR and EEAA remained significantly higher in HIV-1-infected individuals compared with uninfected individuals. We further examined for global patterns of methylation differences between HIV-1-infected and uninfected at each time point, and found 14 groups of co-methylated CpGs that were significantly different between groups at baseline, and remained different after the initiation of ART. Conclusion: We confirm that epigenetic age acceleration associated with HIV-1 infection is most dramatic before ART initiation, and this observation is consistent across four epigenetic clock measurements, as well as in additional groups of co-methylated CpGs identified using WGCNA. Following initiation of ART, there is a partial reduction in age acceleration in all measures, with loss of any significant difference in PEAA and GEAA between serostatus groups. Our findings support the need for future studies examining for a link between epigenetic age acceleration and clinical outcomes in HIV-1-infected individuals.},
	number = {1},
	urldate = {2020-11-18},
	journal = {Pathogens and Immunity},
	author = {Sehl, Mary E. and Rickabaugh, Tammy M. and Shih, Roger and Martinez-Maza, Otoniel and Horvath, Steve and Ramirez, Christina M. and Jamieson, Beth D.},
	month = oct,
	year = {2020},
	pages = {291},
}

Background: HIV-1 infection is associated with acceleration of age-related methylation patterns in peripheral blood and brain of infected individuals although the relative contributions of HIV-1 infection versus its treatment to the observed accelerations in biological aging have not yet been investigated. Methods: In this longitudinal study of the effects of antiretroviral therapy (ART) on epigenetic aging patterns, we extracted DNA from peripheral blood mononuclear cells from 15 HIV-1-infected individuals infected at three time points: 6 months-1year pre-ART, 6-12 months post-initiation of ART, and 18-24 months after initiating ART. We compared these trajectories with those of 15 age-matched uninfected control participants at three time points with similar intervals. Methylation studies were performed using the Infinium methylation 450 arrays. We examined four epigenetic clock measurements: Age acceleration residual (AAR), Extrinsic (EEAA), Phenotypic (PEAA), and Grim (GEAA) epigenetic age acceleration. Weighted correlation network (WGCNA) analysis was used to identify clusters of highly co-methylated CpGs. Results: We found that prior to the initiation of ART all four epigenetic measures were significantly higher in HIV-1-infected individuals compared with uninfected individuals (P\textless0.001 for AAR, P=0.008 for EEAA, P=0.012 for GEAA, P\textless0.001 for PEAA using Wilcoxon rank sum tests between serostatus groups). These effects persisted after the initiation of ART, although the magnitude of these differences diminished. At 18-24 months post-ART initiation (time point 3), PEAA and GEAA were no longer significantly different between HIV-1-infected and uninfected individuals (P=0.059 for PEAA, P=0.11 for GEAA), while AAR and EEAA remained significantly higher in HIV-1-infected individuals compared with uninfected individuals. We further examined for global patterns of methylation differences between HIV-1-infected and uninfected at each time point, and found 14 groups of co-methylated CpGs that were significantly different between groups at baseline, and remained different after the initiation of ART. Conclusion: We confirm that epigenetic age acceleration associated with HIV-1 infection is most dramatic before ART initiation, and this observation is consistent across four epigenetic clock measurements, as well as in additional groups of co-methylated CpGs identified using WGCNA. Following initiation of ART, there is a partial reduction in age acceleration in all measures, with loss of any significant difference in PEAA and GEAA between serostatus groups. Our findings support the need for future studies examining for a link between epigenetic age acceleration and clinical outcomes in HIV-1-infected individuals.

@article{leng_aging_2020,
	title = {Aging, sex, inflammation, frailty, and {CMV} and {HIV} infections},
	volume = {348},
	issn = {00088749},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S0008874919304794},
	doi = {10.1016/j.cellimm.2019.104024},
	language = {en},
	urldate = {2020-11-18},
	journal = {Cellular Immunology},
	author = {Leng, Sean X. and Margolick, Joseph B.},
	month = feb,
	year = {2020},
	pages = {104024},
}

@article{gabuzda_pathogenesis_2020,
	title = {Pathogenesis of {Aging} and {Age}-related {Comorbidities} in {People} with {HIV}: {Highlights} from the {HIV} {ACTION} {Workshop}},
	volume = {5},
	issn = {2469-2964},
	shorttitle = {Pathogenesis of {Aging} and {Age}-related {Comorbidities} in {People} with {HIV}},
	url = {https://paijournal.com/index.php/paijournal/article/view/365},
	doi = {10.20411/pai.v5i1.365},
	abstract = {People with HIV (PWH) experience accentuated biological aging, as defined by markers of inflammation, immune dysfunction, and the epigenetic clock. They also have an elevated risk of multiple age-associated comorbidities. To discuss current knowledge, research gaps, and priorities in aging and age-related comorbidities in treated HIV infection, the NIH program staff organized a workshop held in Bethesda, Maryland in September 2019. This review article describes highlights of discussions led by the Pathogenesis/Basic Science Research working group that focused on three high priority topics: immunopathogenesis; the microbiome/virome; and aging and senescence. We summarize knowledge in these fields and describe key questions for research on the pathogenesis of aging and age-related comorbidities in PWH. Understanding the drivers and mechanisms underlying accentuated biological aging is a high priority that will help identify potential therapeutic targets to improve healthspan in older PWH.},
	number = {1},
	urldate = {2020-11-18},
	journal = {Pathogens and Immunity},
	author = {Gabuzda, Dana and Jamieson, Beth D. and Collman, Ronald G. and Lederman, Michael M. and Burdo, Tricia H. and Deeks, Steven G. and Dittmer, Dirk P. and Fox, Howard S. and Funderburg, Nicholas T. and Pahwa, Savita G. and Pandrea, Ivona and Wilson, Cara C. and Hunt, Peter W.},
	month = jun,
	year = {2020},
	pages = {143},
}

People with HIV (PWH) experience accentuated biological aging, as defined by markers of inflammation, immune dysfunction, and the epigenetic clock. They also have an elevated risk of multiple age-associated comorbidities. To discuss current knowledge, research gaps, and priorities in aging and age-related comorbidities in treated HIV infection, the NIH program staff organized a workshop held in Bethesda, Maryland in September 2019. This review article describes highlights of discussions led by the Pathogenesis/Basic Science Research working group that focused on three high priority topics: immunopathogenesis; the microbiome/virome; and aging and senescence. We summarize knowledge in these fields and describe key questions for research on the pathogenesis of aging and age-related comorbidities in PWH. Understanding the drivers and mechanisms underlying accentuated biological aging is a high priority that will help identify potential therapeutic targets to improve healthspan in older PWH.

@article{fleming_us_2020,
	title = {U.{S}. {Hospitalization} rates and reasons stratified by age among persons with {HIV} 2014–15},
	volume = {32},
	issn = {0954-0121, 1360-0451},
	url = {https://www.tandfonline.com/doi/full/10.1080/09540121.2019.1698705},
	doi = {10.1080/09540121.2019.1698705},
	language = {en},
	number = {11},
	urldate = {2020-11-18},
	journal = {AIDS Care},
	author = {Fleming, Julia and Berry, Stephen A. and Moore, Richard D. and Nijhawan, Ank and Somboonwit, Charurut and Cheever, Laura and Gebo, Kelly A. and {HIV Research Network}},
	month = nov,
	year = {2020},
	pages = {1353--1362},
}

@article{collins_clinical_2020,
	title = {Clinical characteristics, comorbidities and outcomes among persons with {HIV} hospitalized with coronavirus disease 2019 in {Atlanta}, {Georgia}},
	volume = {34},
	issn = {0269-9370, 1473-5571},
	url = {https://journals.lww.com/10.1097/QAD.0000000000002632},
	doi = {10.1097/QAD.0000000000002632},
	language = {en},
	number = {12},
	urldate = {2020-11-18},
	journal = {AIDS},
	author = {Collins, Lauren F. and Moran, Caitlin A. and Oliver, Nora T. and Moanna, Abeer and Lahiri, Cecile D. and Colasanti, Jonathan A. and Kelley, Colleen F. and Nguyen, Minh L. and Marconi, Vincent C. and Armstrong, Wendy S. and Ofotokun, Ighovwerha and Sheth, Anandi N.},
	month = oct,
	year = {2020},
	pages = {1789--1794},
}

@article{kelly_frailty_2019,
	title = {Frailty {Is} an {Independent} {Risk} {Factor} for {Mortality}, {Cardiovascular} {Disease}, {Bone} {Disease}, and {Diabetes} {Among} {Aging} {Adults} {With} {Human} {Immunodeficiency} {Virus}},
	volume = {69},
	issn = {1058-4838, 1537-6591},
	url = {https://academic.oup.com/cid/article/69/8/1370/5258114},
	doi = {10.1093/cid/ciy1101},
	abstract = {Abstract 
             
              Background 
              We characterized associations between frailty and incident cardiovascular disease (CVD), diabetes mellitus (DM), bone disease, and mortality within a cohort of aging persons with human immunodeficiency virus (PWH). 
             
             
              Methods 
              Participants underwent frailty evaluations using the Fried frailty assessment (baseline and annually). Frailty was defined as having ≥3 frailty criteria. Clinical outcomes of mortality, CVD events, DM, and bone disease events were recorded throughout the study period (baseline to most recent study or clinic visit, or date of clinical outcome, whichever came first). Poisson regression models were used to evaluate associations between baseline frailty, change in frailty score over 48 weeks, and each clinical outcome. 
             
             
              Results 
              Among 821 men and 195 women (median age 51 years), 62 (6\%) were frail at baseline. Frailty scores increased by ≥1 component among 194 participants (19\%) from baseline to 48 weeks. Baseline frailty was associated with an increased risk of incident CVD and DM, with a trend toward a significant association with bone events. Among frailty components, slow gait speed was associated with incident DM and borderline associated with incident CVD. An increase in frailty from baseline to week 48 was associated with mortality but not with the other clinical outcomes. 
             
             
              Conclusions 
              Baseline frailty was associated with multiple adverse health outcomes (incident CVD, DM, and bone disease), while increase in frailty score was associated with mortality among PWH engaged in care. Incorporation of frailty assessments into the care of PWH may assist in improvement of functional status and risk stratification for age-related chronic diseases.},
	language = {en},
	number = {8},
	urldate = {2021-09-19},
	journal = {Clinical Infectious Diseases},
	author = {Kelly, Sean G and Wu, Kunling and Tassiopoulos, Katherine and Erlandson, Kristine M and Koletar, Susan L and Palella, Frank J},
	month = sep,
	year = {2019},
	pages = {1370--1376},
}

Abstract Background We characterized associations between frailty and incident cardiovascular disease (CVD), diabetes mellitus (DM), bone disease, and mortality within a cohort of aging persons with human immunodeficiency virus (PWH). Methods Participants underwent frailty evaluations using the Fried frailty assessment (baseline and annually). Frailty was defined as having ≥3 frailty criteria. Clinical outcomes of mortality, CVD events, DM, and bone disease events were recorded throughout the study period (baseline to most recent study or clinic visit, or date of clinical outcome, whichever came first). Poisson regression models were used to evaluate associations between baseline frailty, change in frailty score over 48 weeks, and each clinical outcome. Results Among 821 men and 195 women (median age 51 years), 62 (6%) were frail at baseline. Frailty scores increased by ≥1 component among 194 participants (19%) from baseline to 48 weeks. Baseline frailty was associated with an increased risk of incident CVD and DM, with a trend toward a significant association with bone events. Among frailty components, slow gait speed was associated with incident DM and borderline associated with incident CVD. An increase in frailty from baseline to week 48 was associated with mortality but not with the other clinical outcomes. Conclusions Baseline frailty was associated with multiple adverse health outcomes (incident CVD, DM, and bone disease), while increase in frailty score was associated with mortality among PWH engaged in care. Incorporation of frailty assessments into the care of PWH may assist in improvement of functional status and risk stratification for age-related chronic diseases.

@article{webel_physical_2019,
	title = {Physical {Activity} {Intensity} is {Associated} with {Symptom} {Distress} in the {CNICS} {Cohort}},
	volume = {23},
	issn = {1090-7165, 1573-3254},
	url = {http://link.springer.com/10.1007/s10461-018-2319-7},
	doi = {10.1007/s10461-018-2319-7},
	language = {en},
	number = {3},
	urldate = {2020-11-18},
	journal = {AIDS and Behavior},
	author = {Webel, Allison R. and Willig, Amanda L. and Liu, Wei and Sattar, Abdus and Boswell, Stephen and Crane, Heidi M. and Hunt, Peter and Kitahata, Mari and Matthews, W. Christopher and Saag, Michael S. and Lederman, Michael M. and Rodriguez, Benigno},
	month = mar,
	year = {2019},
	pages = {627--635},
}

@article{kong_non-hiv_2019,
	title = {Non-{HIV} {Comorbid} {Conditions} and {Polypharmacy} {Among} {People} {Living} with {HIV} {Age} 65 or {Older} {Compared} with {HIV}-{Negative} {Individuals} {Age} 65 or {Older} in the {United} {States}: {A} {Retrospective} {Claims}-{Based} {Analysis}},
	volume = {33},
	issn = {1087-2914, 1557-7449},
	shorttitle = {Non-{HIV} {Comorbid} {Conditions} and {Polypharmacy} {Among} {People} {Living} with {HIV} {Age} 65 or {Older} {Compared} with {HIV}-{Negative} {Individuals} {Age} 65 or {Older} in the {United} {States}},
	url = {https://www.liebertpub.com/doi/10.1089/apc.2018.0190},
	doi = {10.1089/apc.2018.0190},
	language = {en},
	number = {3},
	urldate = {2020-11-18},
	journal = {AIDS Patient Care and STDs},
	author = {Kong, Amanda M. and Pozen, Alexis and Anastos, Kathryn and Kelvin, Elizabeth A. and Nash, Denis},
	month = mar,
	year = {2019},
	pages = {93--103},
}

@article{de_francesco_people_2019,
	title = {Do people living with {HIV} experience greater age advancement than their {HIV}-negative counterparts?:},
	volume = {33},
	issn = {0269-9370},
	shorttitle = {Do people living with {HIV} experience greater age advancement than their {HIV}-negative counterparts?},
	url = {http://journals.lww.com/00002030-201902010-00009},
	doi = {10.1097/QAD.0000000000002063},
	language = {en},
	number = {2},
	urldate = {2020-11-18},
	journal = {AIDS},
	author = {De Francesco, Davide and Wit, Ferdinand W. and Bürkle, Alexander and Oehlke, Sebastian and Kootstra, Neeltje A. and Winston, Alan and Franceschi, Claudio and Garagnani, Paolo and Pirazzini, Chiara and Libert, Claude and Grune, Tilman and Weber, Daniela and Jansen, Eugène H.J.M. and Sabin, Caroline A. and Reiss, Peter},
	month = feb,
	year = {2019},
	pages = {259--268},
}

@article{crane_physical_2019,
	title = {Physical {Functioning} {Among} {Patients} {Aging} {With} {Human} {Immunodeficiency} {Virus} ({HIV}) {Versus} {HIV} {Uninfected}: {Feasibility} of {Using} the {Short} {Physical} {Performance} {Battery} in {Clinical} {Care} of {People} {Living} {With} {HIV} {Aged} 50 or {Older}},
	volume = {6},
	issn = {2328-8957},
	shorttitle = {Physical {Functioning} {Among} {Patients} {Aging} {With} {Human} {Immunodeficiency} {Virus} ({HIV}) {Versus} {HIV} {Uninfected}},
	url = {https://academic.oup.com/ofid/article/doi/10.1093/ofid/ofz038/5374626},
	doi = {10.1093/ofid/ofz038},
	abstract = {Abstract 
             
              Background 
              The Short Physical Performance Battery (SPPB) is a well regarded physical functioning assessment including balance, gait speed, and chair-stand tests. Its use has not been widely assessed in human immunodeficiency virus (HIV) care. We evaluated the feasibility of integrating the SPPB into care of aging people living with HIV (PLWH) and compared SPPB performance with aged HIV-uninfected individuals. 
             
             
              Methods 
              We enrolled PLWH aged ≥50 at 3 HIV clinics and compared their SPPB scores and subscores with older HIV-uninfected adults in the Health, Aging, and Body Composition (Health ABC) study. We conducted regression analyses on age stratified by sex and adjusting for site, and we calculated percentage variance explained by age among PLWH and HIV-uninfected adults. 
             
             
              Results 
              The SPPB was feasible to implement in clinical care and did not require licensed professionals; 176 PLWH completed it with a mean completion time of 7.0 minutes (standard deviation = 2.6). Overall mean SPPB score among PLWH was 10.3 (median 11.0, 25th percentile 9.0, 75th percentile 12.0). People living with HIV were younger than HIV-uninfected individuals (55 vs 74 years old). Mean SPPB scores and most subscores were similar among PLWH and older HIV-uninfected individuals despite the {\textasciitilde}20-year age difference. Regression analyses of gait speed revealed similar slopes in PLWH and HIV-uninfected individuals; however, separate intercepts were needed for PLWH. Mean gait speeds were faster in older HIV-uninfected men and women (P \< .01), yet relationships with age within PLWH and HIV uninfected were similar. 
             
             
              Conclusions 
              The SPPB can be implemented into busy HIV clinics. Despite the {\textasciitilde}20-year age difference, mean scores were similar among PLWH and older HIV-uninfected individuals, although gait speed was faster among HIV-uninfected individuals.},
	language = {en},
	number = {3},
	urldate = {2020-11-18},
	journal = {Open Forum Infectious Diseases},
	author = {Crane, Heidi M and Miller, Michael E and Pierce, June and Willig, Amanda L and Case, Michael Lloyd and Wilkin, Aimee M and Brown, Sharon and Asirot, Mary Grace and Fredericksen, Rob J and Saag, Michael S and Landay, Alan L and High, Kevin P},
	month = mar,
	year = {2019},
	pages = {ofz038},
}

Abstract Background The Short Physical Performance Battery (SPPB) is a well regarded physical functioning assessment including balance, gait speed, and chair-stand tests. Its use has not been widely assessed in human immunodeficiency virus (HIV) care. We evaluated the feasibility of integrating the SPPB into care of aging people living with HIV (PLWH) and compared SPPB performance with aged HIV-uninfected individuals. Methods We enrolled PLWH aged ≥50 at 3 HIV clinics and compared their SPPB scores and subscores with older HIV-uninfected adults in the Health, Aging, and Body Composition (Health ABC) study. We conducted regression analyses on age stratified by sex and adjusting for site, and we calculated percentage variance explained by age among PLWH and HIV-uninfected adults. Results The SPPB was feasible to implement in clinical care and did not require licensed professionals; 176 PLWH completed it with a mean completion time of 7.0 minutes (standard deviation = 2.6). Overall mean SPPB score among PLWH was 10.3 (median 11.0, 25th percentile 9.0, 75th percentile 12.0). People living with HIV were younger than HIV-uninfected individuals (55 vs 74 years old). Mean SPPB scores and most subscores were similar among PLWH and older HIV-uninfected individuals despite the ~20-year age difference. Regression analyses of gait speed revealed similar slopes in PLWH and HIV-uninfected individuals; however, separate intercepts were needed for PLWH. Mean gait speeds were faster in older HIV-uninfected men and women (P < .01), yet relationships with age within PLWH and HIV uninfected were similar. Conclusions The SPPB can be implemented into busy HIV clinics. Despite the ~20-year age difference, mean scores were similar among PLWH and older HIV-uninfected individuals, although gait speed was faster among HIV-uninfected individuals.

@article{wong_multimorbidity_2018,
	title = {Multimorbidity {Among} {Persons} {Living} with {Human} {Immunodeficiency} {Virus} in the {United} {States}},
	volume = {66},
	issn = {1058-4838, 1537-6591},
	url = {https://academic.oup.com/cid/article/66/8/1230/4628146},
	doi = {10.1093/cid/cix998},
	language = {en},
	number = {8},
	urldate = {2020-11-18},
	journal = {Clinical Infectious Diseases},
	author = {Wong, Cherise and Gange, Stephen J and Moore, Richard D and Justice, Amy C and Buchacz, Kate and Abraham, Alison G and Rebeiro, Peter F and Koethe, John R and Martin, Jeffrey N and Horberg, Michael A and Boyd, Cynthia M and Kitahata, Mari M and Crane, Heidi M and Gebo, Kelly A and Gill, M John and Silverberg, Michael J and Palella, Frank J and Patel, Pragna and Samji, Hasina and Thorne, Jennifer and Rabkin, Charles S and Mayor, Angel and Althoff, Keri N and {North American AIDS Cohort Collaboration on Research and Design (NA-ACCORD)} and Freeman, Aimee M and Cescon, Angela and Rachlis, Anita R and Rogers, Ben and Rodriguez, Benigno and Grasso, Chris and Benson, Constance A and Drozd, Daniel R and Fiellin, David and Haas, David and Kirk, Gregory D and Willig, James and Globerman, Jason and Brooks, John T and Eron, Joseph J and Montaner, Julio SG and Gabler, Karyn and Anastos, Kathryn and Mayer, Kenneth H and Jacobson, Lisa P and Kopansky-Giles, Madison and Klein, Marina B and Turner, Megan and Mugavero, Michael J and Saag, Michael S and Harrigan, P Richard and Dubrow, Robert and Hunter-Mellado, Robert F and Hogg, Robert S and Bosch, Ronald J and McKaig, Rosemary G and Bebawy, Sally and Rourke, Sean B and Napravnik, Sonia and Boswell, Stephen and Sterling, Timothy R},
	month = apr,
	year = {2018},
	pages = {1230--1238},
}

@article{margolick_relationship_2018,
	title = {Relationship {Between} {T}-{Cell} {Responses} to {CMV}, {Markers} of {Inflammation}, and {Frailty} in {HIV}-uninfected and {HIV}-infected {Men} in the {Multicenter} {AIDS} {Cohort} {Study}},
	volume = {218},
	issn = {0022-1899, 1537-6613},
	url = {https://academic.oup.com/jid/article/218/2/249/4909741},
	doi = {10.1093/infdis/jiy005},
	language = {en},
	number = {2},
	urldate = {2020-11-18},
	journal = {The Journal of Infectious Diseases},
	author = {Margolick, Joseph B and Bream, Jay H and Nilles, Tricia L and Li, Huifen and Langan, Susan J and Deng, Shane and Wang, Ruibin and Wada, Nikolas and Leng, Sean X},
	month = jun,
	year = {2018},
	pages = {249--258},
}

@article{letendre_higher_2018,
	title = {Higher {Anti}-{Cytomegalovirus} {Immunoglobulin} {G} {Concentrations} {Are} {Associated} {With} {Worse} {Neurocognitive} {Performance} {During} {Suppressive} {Antiretroviral} {Therapy}},
	volume = {67},
	issn = {1058-4838, 1537-6591},
	url = {https://academic.oup.com/cid/article/67/5/770/4915913},
	doi = {10.1093/cid/ciy170},
	language = {en},
	number = {5},
	urldate = {2020-11-18},
	journal = {Clinical Infectious Diseases},
	author = {Letendre, Scott and Bharti, Ajay and Perez-Valero, Ignacio and Hanson, Barbara and Franklin, Donald and Woods, Steven Paul and Gianella, Sara and de Oliveira, Michelli Faria and Heaton, Robert K and Grant, Igor and Landay, Alan L and Lurain, Nell and {CNS HIV AntiRetroviral Therapy Effects Research (CHARTER) Group}},
	month = aug,
	year = {2018},
	pages = {770--777},
}

@article{gurau_anti-senescence_2018,
	title = {Anti-senescence compounds: {A} potential nutraceutical approach to healthy aging},
	volume = {46},
	issn = {15681637},
	shorttitle = {Anti-senescence compounds},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S1568163718300199},
	doi = {10.1016/j.arr.2018.05.001},
	language = {en},
	urldate = {2020-11-18},
	journal = {Ageing Research Reviews},
	author = {Gurău, Felicia and Baldoni, Simone and Prattichizzo, Francesco and Espinosa, Emma and Amenta, Francesco and Procopio, Antonio Domenico and Albertini, Maria Cristina and Bonafè, Massimiliano and Olivieri, Fabiola},
	month = sep,
	year = {2018},
	pages = {14--31},
}

@article{johs_disability_2017,
	title = {Disability {Among} {Middle}-{Aged} and {Older} {Persons} {With} {Human} {Immunodeficiency} {Virus} {Infection}},
	volume = {65},
	issn = {1058-4838, 1537-6591},
	url = {https://academic.oup.com/cid/article/65/1/83/3091379},
	doi = {10.1093/cid/cix253},
	language = {en},
	number = {1},
	urldate = {2021-09-19},
	journal = {Clinical Infectious Diseases},
	author = {Johs, Nikolas A and Wu, Kunling and Tassiopoulos, Katherine and Koletar, Susan L and Kalayjian, Robert C and Ellis, Ronald J and Taiwo, Babafemi and Palella, Frank J and Erlandson, Kristine M},
	month = jul,
	year = {2017},
	pages = {83--91},
}

@article{sabin_epidemiology_2017,
	title = {Epidemiology of ageing with {HIV}: what can we learn from cohorts?},
	volume = {31},
	issn = {0269-9370},
	shorttitle = {Epidemiology of ageing with {HIV}},
	url = {https://journals.lww.com/00002030-201706002-00003},
	doi = {10.1097/QAD.0000000000001374},
	language = {en},
	number = {Supplement 2},
	urldate = {2021-05-11},
	journal = {AIDS},
	author = {Sabin, Caroline A. and Reiss, Peter},
	month = jun,
	year = {2017},
	pages = {S121--S128},
}

@article{willig_monocyte_2017,
	title = {Monocyte bioenergetic function is associated with body composition in virologically suppressed {HIV}-infected women},
	volume = {12},
	issn = {22132317},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S2213231717300381},
	doi = {10.1016/j.redox.2017.04.005},
	language = {en},
	urldate = {2020-11-18},
	journal = {Redox Biology},
	author = {Willig, Amanda L. and Kramer, Philip A. and Chacko, Balu K. and Darley-Usmar, Victor M. and Heath, Sonya L. and Overton, E. Turner},
	month = aug,
	year = {2017},
	pages = {648--656},
}

@article{noorhasan_associations_2017,
	title = {Associations {Between} {At}-{Risk} {Alcohol} {Use}, {Substance} {Use}, and {Smoking} with {Lipohypertrophy} and {Lipoatrophy} {Among} {Patients} {Living} with {HIV}},
	volume = {33},
	issn = {0889-2229, 1931-8405},
	url = {http://www.liebertpub.com/doi/10.1089/aid.2015.0357},
	doi = {10.1089/aid.2015.0357},
	language = {en},
	number = {6},
	urldate = {2020-11-18},
	journal = {AIDS Research and Human Retroviruses},
	author = {Noorhasan, Marisela and Drozd, Daniel R. and Grunfeld, Carl and Merrill, Joseph O. and Burkholder, Greer A. and Mugavero, Michael J. and Willig, James H. and Willig, Amanda L. and Cropsey, Karen L. and Mayer, Kenneth H. and Blashill, Aaron and Mimiaga, Matthew and McCaul, Mary E. and Hutton, Heidi and Chander, Geetanjali and Mathews, William C. and Napravnik, Sonia and Eron, Joseph J. and Christopoulos, Katerina and Fredericksen, Rob J. and Nance, Robin M. and Delaney, Joseph Chris and Crane, Paul K. and Saag, Michael S. and Kitahata, Mari M. and Crane, Heidi M. and {on behalf of the Centers For AIDS R}},
	month = jun,
	year = {2017},
	pages = {534--545},
}

@article{drozd_increased_2017,
	title = {Increased {Risk} of {Myocardial} {Infarction} in {HIV}-{Infected} {Individuals} in {North} {America} {Compared} {With} the {General} {Population}:},
	volume = {75},
	issn = {1525-4135},
	shorttitle = {Increased {Risk} of {Myocardial} {Infarction} in {HIV}-{Infected} {Individuals} in {North} {America} {Compared} {With} the {General} {Population}},
	url = {http://journals.lww.com/00126334-201708150-00011},
	doi = {10.1097/QAI.0000000000001450},
	language = {en},
	number = {5},
	urldate = {2020-11-18},
	journal = {JAIDS Journal of Acquired Immune Deficiency Syndromes},
	author = {Drozd, Daniel R. and Kitahata, Mari M. and Althoff, Keri N. and Zhang, Jinbing and Gange, Stephen J. and Napravnik, Sonia and Burkholder, Greer A. and Mathews, William C. and Silverberg, Michael J. and Sterling, Timothy R. and Heckbert, Susan R. and Budoff, Matthew J. and Van Rompaey, Stephen and Delaney, Joseph A.C. and Wong, Cherise and Tong, Weiqun and Palella, Frank J. and Elion, Richard A. and Martin, Jeffrey N. and Brooks, John T. and Jacobson, Lisa P. and Eron, Joseph J. and Justice, Amy C. and Freiberg, Matthew S. and Klein, Daniel B. and Post, Wendy S. and Saag, Michael S. and Moore, Richard D. and Crane, Heidi M.},
	month = aug,
	year = {2017},
	pages = {568--576},
}

@article{trickey_cause-specific_2016,
	title = {Cause-{Specific} {Mortality} in {HIV}-{Positive} {Patients} {Who} {Survived} {Ten} {Years} after {Starting} {Antiretroviral} {Therapy}},
	volume = {11},
	issn = {1932-6203},
	url = {https://dx.plos.org/10.1371/journal.pone.0160460},
	doi = {10.1371/journal.pone.0160460},
	language = {en},
	number = {8},
	urldate = {2020-11-18},
	journal = {PLOS ONE},
	author = {Trickey, Adam and May, Margaret T. and Vehreschild, Janne and Obel, Niels and Gill, Michael John and Crane, Heidi and Boesecke, Christoph and Samji, Hasina and Grabar, Sophie and Cazanave, Charles and Cavassini, Matthias and Shepherd, Leah and d’Arminio Monforte, Antonella and Smit, Colette and Saag, Michael and Lampe, Fiona and Hernando, Vicky and Montero, Marta and Zangerle, Robert and Justice, Amy C. and Sterling, Timothy and Miro, Jose and Ingle, Suzanne and Sterne, Jonathan A. C. and {Antiretroviral Therapy Cohort Collaboration (ART-CC)}},
	editor = {Speck, Roberto F.},
	month = aug,
	year = {2016},
	pages = {e0160460},
}

@article{sierra_moving_2016,
	title = {Moving {Geroscience} {Into} {Uncharted} {Waters}},
	volume = {71},
	issn = {1079-5006},
	url = {https://academic.oup.com/biomedgerontology/article/71/11/1385/2400009},
	doi = {10.1093/gerona/glw087},
	abstract = {Research into the basic biology of aging has undergone a seismic shift in the last 10–20 years, moving rapidly from the very descriptive approach focused on the},
	language = {en},
	number = {11},
	urldate = {2020-11-18},
	journal = {The Journals of Gerontology: Series A},
	author = {Sierra, Felipe},
	month = nov,
	year = {2016},
	pages = {1385--1387},
}

Research into the basic biology of aging has undergone a seismic shift in the last 10–20 years, moving rapidly from the very descriptive approach focused on the

@article{seals_physiological_2016,
	title = {Physiological geroscience: targeting function to increase healthspan and achieve optimal longevity: {Translational} physiology of ageing},
	volume = {594},
	issn = {00223751},
	shorttitle = {Physiological geroscience},
	url = {http://doi.wiley.com/10.1113/jphysiol.2014.282665},
	doi = {10.1113/jphysiol.2014.282665},
	language = {en},
	number = {8},
	urldate = {2020-11-18},
	journal = {The Journal of Physiology},
	author = {Seals, Douglas R. and Justice, Jamie N. and LaRocca, Thomas J.},
	month = apr,
	year = {2016},
	pages = {2001--2024},
}

@article{park_prevalence_2016,
	title = {Prevalence of non-{HIV} cancer risk factors in persons living with {HIV}/{AIDS}: a meta-analysis},
	volume = {30},
	issn = {0269-9370},
	shorttitle = {Prevalence of non-{HIV} cancer risk factors in persons living with {HIV}/{AIDS}},
	url = {http://journals.lww.com/00002030-201601140-00014},
	doi = {10.1097/QAD.0000000000000922},
	language = {en},
	number = {2},
	urldate = {2020-11-18},
	journal = {AIDS},
	author = {Park, Lesley S. and Hernández-Ramírez, Raúl U. and Silverberg, Michael J. and Crothers, Kristina and Dubrow, Robert},
	month = jan,
	year = {2016},
	pages = {273--291},
}

@article{melov_geroscience_2016,
	title = {Geroscience approaches to increase healthspan and slow aging},
	volume = {5},
	issn = {2046-1402},
	url = {https://f1000research.com/articles/5-785/v1},
	doi = {10.12688/f1000research.7583.1},
	abstract = {For decades, researchers in the biology of aging have focused on defining mechanisms that modulate aging by primarily studying a single metric, sometimes described as the “gold standard” lifespan. Increasingly, geroscience research is turning towards defining functional domains of aging such as the cardiovascular system, skeletal integrity, and metabolic health as being a more direct route to understand why tissues decline in function with age. Each model used in aging research has strengths and weaknesses, yet we know surprisingly little about how critical tissues decline in health with increasing age. Here I discuss popular model systems used in geroscience research and their utility as possible tools in preclinical studies in aging.},
	language = {en},
	urldate = {2020-11-18},
	journal = {F1000Research},
	author = {Melov, Simon},
	month = apr,
	year = {2016},
	pages = {785},
}

For decades, researchers in the biology of aging have focused on defining mechanisms that modulate aging by primarily studying a single metric, sometimes described as the “gold standard” lifespan. Increasingly, geroscience research is turning towards defining functional domains of aging such as the cardiovascular system, skeletal integrity, and metabolic health as being a more direct route to understand why tissues decline in function with age. Each model used in aging research has strengths and weaknesses, yet we know surprisingly little about how critical tissues decline in health with increasing age. Here I discuss popular model systems used in geroscience research and their utility as possible tools in preclinical studies in aging.

@incollection{sierra_hiv_2016,
	address = {Cham},
	title = {{HIV} and {Aging}: {Parallels} and {Synergistic} {Mechanisms} {Leading} to {Premature} {Disease} and {Functional} {Decline}},
	isbn = {9783319232454 9783319232461},
	shorttitle = {{HIV} and {Aging}},
	url = {http://link.springer.com/10.1007/978-3-319-23246-1_17},
	language = {en},
	urldate = {2020-11-18},
	booktitle = {Advances in {Geroscience}},
	publisher = {Springer International Publishing},
	author = {Hearps, Anna and Schafer, Katherine and High, Kevin and Landay, Alan},
	editor = {Sierra, Felipe and Kohanski, Ronald},
	year = {2016},
	doi = {10.1007/978-3-319-23246-1_17},
	pages = {509--550},
}

@article{horvath_hiv-1_2015,
	title = {{HIV}-1 {Infection} {Accelerates} {Age} {According} to the {Epigenetic} {Clock}},
	volume = {212},
	issn = {0022-1899, 1537-6613},
	url = {https://academic.oup.com/jid/article-lookup/doi/10.1093/infdis/jiv277},
	doi = {10.1093/infdis/jiv277},
	language = {en},
	number = {10},
	urldate = {2020-11-18},
	journal = {Journal of Infectious Diseases},
	author = {Horvath, Steve and Levine, Andrew J.},
	month = nov,
	year = {2015},
	pages = {1563--1573},
}

@article{greene_geriatric_2015,
	title = {Geriatric {Syndromes} in {Older} {HIV}-{Infected} {Adults}:},
	volume = {69},
	issn = {1525-4135},
	shorttitle = {Geriatric {Syndromes} in {Older} {HIV}-{Infected} {Adults}},
	url = {http://journals.lww.com/00126334-201506010-00005},
	doi = {10.1097/QAI.0000000000000556},
	language = {en},
	number = {2},
	urldate = {2020-11-18},
	journal = {JAIDS Journal of Acquired Immune Deficiency Syndromes},
	author = {Greene, Meredith and Covinsky, Kenneth E. and Valcour, Victor and Miao, Yinghui and Madamba, Joy and Lampiris, Harry and Cenzer, Irena Stijacic and Martin, Jeffrey and Deeks, Steven G.},
	month = jun,
	year = {2015},
	pages = {161--167},
}

@article{kendall_cross-sectional_2014,
	title = {A cross-sectional, population-based study measuring comorbidity among people living with {HIV} in {Ontario}},
	volume = {14},
	issn = {1471-2458},
	url = {http://bmcpublichealth.biomedcentral.com/articles/10.1186/1471-2458-14-161},
	doi = {10.1186/1471-2458-14-161},
	language = {en},
	number = {1},
	urldate = {2020-11-18},
	journal = {BMC Public Health},
	author = {Kendall, Claire E and Wong, Jenna and Taljaard, Monica and Glazier, Richard H and Hogg, William and Younger, Jaime and Manuel, Douglas G},
	month = dec,
	year = {2014},
	pages = {161},
}

@article{weber_decreasing_2013,
	title = {Decreasing mortality and changing patterns of causes of death in the {Swiss} {HIV} {Cohort} {Study}: {Causes} of death and {HIV} infection},
	volume = {14},
	issn = {14642662},
	shorttitle = {Decreasing mortality and changing patterns of causes of death in the {Swiss} {HIV} {Cohort} {Study}},
	url = {http://doi.wiley.com/10.1111/j.1468-1293.2012.01051.x},
	doi = {10.1111/j.1468-1293.2012.01051.x},
	language = {en},
	number = {4},
	urldate = {2020-11-18},
	journal = {HIV Medicine},
	author = {Weber, R and Ruppik, M and Rickenbach, M and Spoerri, A and Furrer, H and Battegay, M and Cavassini, M and Calmy, A and Bernasconi, E and Schmid, P and Flepp, M and Kowalska, J and Ledergerber, B and {Swiss HIV Cohort Study (SHCS)}},
	month = apr,
	year = {2013},
	pages = {195--207},
}

@article{lopez-otin_hallmarks_2013,
	title = {The {Hallmarks} of {Aging}},
	volume = {153},
	issn = {00928674},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S0092867413006454},
	doi = {10.1016/j.cell.2013.05.039},
	language = {en},
	number = {6},
	urldate = {2020-11-18},
	journal = {Cell},
	author = {López-Otín, Carlos and Blasco, Maria A. and Partridge, Linda and Serrano, Manuel and Kroemer, Guido},
	month = jun,
	year = {2013},
	pages = {1194--1217},
}

@article{justice_does_2012,
	title = {Does an {Index} {Composed} of {Clinical} {Data} {Reflect} {Effects} of {Inflammation}, {Coagulation}, and {Monocyte} {Activation} on {Mortality} {Among} {Those} {Aging} {With} {HIV}?},
	volume = {54},
	issn = {1058-4838, 1537-6591},
	url = {https://academic.oup.com/cid/article-lookup/doi/10.1093/cid/cir989},
	doi = {10.1093/cid/cir989},
	language = {en},
	number = {7},
	urldate = {2020-11-18},
	journal = {Clinical Infectious Diseases},
	author = {Justice, A. C. and Freiberg, M. S. and Tracy, R. and Kuller, L. and Tate, J. P. and Goetz, M. B. and Fiellin, D. A. and Vanasse, G. J. and Butt, A. A. and Rodriguez-Barradas, M. C. and Gibert, C. and Oursler, K. A. and Deeks, S. G. and Bryant, K. and {the VACS Project Team}},
	month = apr,
	year = {2012},
	pages = {984--994},
}

@article{high_hiv_2012,
	title = {{HIV} and {Aging}: {State} of {Knowledge} and {Areas} of {Critical} {Need} for {Research}. {A} {Report} to the {NIH} {Office} of {AIDS} {Research} by the {HIV} and {Aging} {Working} {Group}},
	volume = {60},
	issn = {1525-4135},
	shorttitle = {{HIV} and {Aging}},
	url = {http://journals.lww.com/00126334-201207011-00001},
	doi = {10.1097/QAI.0b013e31825a3668},
	language = {en},
	urldate = {2020-11-18},
	journal = {JAIDS Journal of Acquired Immune Deficiency Syndromes},
	author = {High, Kevin P. and Brennan-Ing, Mark and Clifford, David B. and Cohen, Mardge H. and Currier, Judith and Deeks, Steven G. and Deren, Sherry and Effros, Rita B. and Gebo, Kelly and Goronzy, Jörg J. and Justice, Amy C. and Landay, Alan and Levin, Jules and Miotti, Paolo G. and Munk, Robert J. and Nass, Heidi and Rinaldo, Charles R. and Shlipak, Michael G. and Tracy, Russell and Valcour, Victor and Vance, David E. and Walston, Jeremy D. and Volberding, Paul},
	month = jul,
	year = {2012},
	pages = {S1--S18},
}

@article{guaraldi_progression_2012,
	title = {Progression of coronary artery calcium in men affected by human immunodeficiency virus infection},
	volume = {28},
	issn = {1569-5794, 1573-0743},
	url = {http://link.springer.com/10.1007/s10554-011-9898-y},
	doi = {10.1007/s10554-011-9898-y},
	language = {en},
	number = {4},
	urldate = {2020-11-18},
	journal = {The International Journal of Cardiovascular Imaging},
	author = {Guaraldi, Giovanni and Zona, Stefano and Orlando, Gabriella and Carli, Federica and Ligabue, Guido and Fiocchi, Federica and Rossi, Rosario and Modena, Maria Grazia and Raggi, Paolo},
	month = apr,
	year = {2012},
	pages = {935--941},
}

@article{womack_increased_2011,
	title = {Increased {Risk} of {Fragility} {Fractures} among {HIV} {Infected} {Compared} to {Uninfected} {Male} {Veterans}},
	volume = {6},
	issn = {1932-6203},
	url = {https://dx.plos.org/10.1371/journal.pone.0017217},
	doi = {10.1371/journal.pone.0017217},
	language = {en},
	number = {2},
	urldate = {2020-11-18},
	journal = {PLoS ONE},
	author = {Womack, Julie A. and Goulet, Joseph L. and Gibert, Cynthia and Brandt, Cynthia and Chang, Chung Chou and Gulanski, Barbara and Fraenkel, Liana and Mattocks, Kristin and Rimland, David and Rodriguez-Barradas, Maria C. and Tate, Janet and Yin, Michael T. and Justice, Amy C. and {for the Veterans Aging Cohort Study Project Team}},
	editor = {Myer, Landon},
	month = feb,
	year = {2011},
	pages = {e17217},
}

@article{silverberg_hiv_2011,
	title = {{HIV} {Infection}, {Immunodeficiency}, {Viral} {Replication}, and the {Risk} of {Cancer}},
	volume = {20},
	issn = {1055-9965, 1538-7755},
	url = {http://cebp.aacrjournals.org/cgi/doi/10.1158/1055-9965.EPI-11-0777},
	doi = {10.1158/1055-9965.EPI-11-0777},
	language = {en},
	number = {12},
	urldate = {2020-11-18},
	journal = {Cancer Epidemiology Biomarkers \& Prevention},
	author = {Silverberg, M. J. and Chao, C. and Leyden, W. A. and Xu, L. and Horberg, M. A. and Klein, D. and Towner, W. J. and Dubrow, R. and Quesenberry, C. P. and Neugebauer, R. S. and Abrams, D. I.},
	month = dec,
	year = {2011},
	pages = {2551--2559},
}

@article{onen_review_2011,
	title = {A review of premature frailty in {HIV}-infected persons; another manifestation of {HIV}-related accelerated aging},
	volume = {4},
	issn = {1874-6128},
	abstract = {PURPOSE: HIV-related immunological and multisystem accelerated aging contributes to the premature occurrence of age-related comorbidities. Such non-AIDS-defining comorbidities include cardiovascular disease, dyslipidemia, osteoporosis and frailty, and are of increasing importance with improved survival on antiretrovirals. This review will describe the underlying pathogenesis of HIV-related accelerated aging and will thereafter focus on frailty, a clinical concept which has only recently been studied in the HIV field.
METHODS: A literature search was performed using PubMed. Cited articles were peer reviewed and included prospective, retrospective and basic science studies, systematic reviews and Center for Disease Control and Prevention data.
RESULTS: HIV infection is characterized profound immune dysregulation, which can hasten cardiovascular, renal, cerebrovascular and bone disease and precede their overt manifestation by years. Viral mediated atherogenesis further accelerates end organ dysfunction and increases mortality. Frailty, a clinical syndrome characterized by multisystem dysregulation and increased vulnerability to stressors, occurs prematurely in HIV-infected persons especially those with advanced disease. Frailty prevalence and clinical characteristics are similar in affected older adults and HIV-infected persons. Its presence is associated with a number of negative outcomes including greater comorbidity and hospitalization.
CONCLUSION: Premature frailty, like other non-AIDS-defining comorbidities, is a manifestation of HIV-related accelerated aging. The synergism of HIV infection and aging has alarming clinical and socioeconomic implications. Research is needed to identify the factors that predict the development of premature frailty among HIV-infected persons and the optimal prevention and management strategies.},
	language = {eng},
	number = {1},
	journal = {Current Aging Science},
	author = {Önen, Nur F. and Overton, E. Turner},
	month = feb,
	year = {2011},
	pmid = {21204781},
	keywords = {Aging, Premature, Comorbidity, HIV Infections, Humans, Prevalence},
	pages = {33--41},
}

PURPOSE: HIV-related immunological and multisystem accelerated aging contributes to the premature occurrence of age-related comorbidities. Such non-AIDS-defining comorbidities include cardiovascular disease, dyslipidemia, osteoporosis and frailty, and are of increasing importance with improved survival on antiretrovirals. This review will describe the underlying pathogenesis of HIV-related accelerated aging and will thereafter focus on frailty, a clinical concept which has only recently been studied in the HIV field. METHODS: A literature search was performed using PubMed. Cited articles were peer reviewed and included prospective, retrospective and basic science studies, systematic reviews and Center for Disease Control and Prevention data. RESULTS: HIV infection is characterized profound immune dysregulation, which can hasten cardiovascular, renal, cerebrovascular and bone disease and precede their overt manifestation by years. Viral mediated atherogenesis further accelerates end organ dysfunction and increases mortality. Frailty, a clinical syndrome characterized by multisystem dysregulation and increased vulnerability to stressors, occurs prematurely in HIV-infected persons especially those with advanced disease. Frailty prevalence and clinical characteristics are similar in affected older adults and HIV-infected persons. Its presence is associated with a number of negative outcomes including greater comorbidity and hospitalization. CONCLUSION: Premature frailty, like other non-AIDS-defining comorbidities, is a manifestation of HIV-related accelerated aging. The synergism of HIV infection and aging has alarming clinical and socioeconomic implications. Research is needed to identify the factors that predict the development of premature frailty among HIV-infected persons and the optimal prevention and management strategies.

@article{hasse_morbidity_2011,
	title = {Morbidity and {Aging} in {HIV}-{Infected} {Persons}: {The} {Swiss} {HIV} {Cohort} {Study}},
	volume = {53},
	issn = {1058-4838, 1537-6591},
	shorttitle = {Morbidity and {Aging} in {HIV}-{Infected} {Persons}},
	url = {https://academic.oup.com/cid/article-lookup/doi/10.1093/cid/cir626},
	doi = {10.1093/cid/cir626},
	language = {en},
	number = {11},
	urldate = {2020-11-18},
	journal = {Clinical Infectious Diseases},
	author = {Hasse, B. and Ledergerber, B. and Furrer, H. and Battegay, M. and Hirschel, B. and Cavassini, M. and Bertisch, B. and Bernasconi, E. and Weber, R. and {the Swiss HIV Cohort Study}},
	month = dec,
	year = {2011},
	pages = {1130--1139},
}

@article{guaraldi_premature_2011,
	title = {Premature {Age}-{Related} {Comorbidities} {Among} {HIV}-{Infected} {Persons} {Compared} {With} the {General} {Population}},
	volume = {53},
	issn = {1058-4838, 1537-6591},
	url = {https://academic.oup.com/cid/article-lookup/doi/10.1093/cid/cir627},
	doi = {10.1093/cid/cir627},
	language = {en},
	number = {11},
	urldate = {2020-11-18},
	journal = {Clinical Infectious Diseases},
	author = {Guaraldi, G. and Orlando, G. and Zona, S. and Menozzi, M. and Carli, F. and Garlassi, E. and Berti, A. and Rossi, E. and Roverato, A. and Palella, F.},
	month = dec,
	year = {2011},
	pages = {1120--1126},
}

@article{durand_association_2011,
	title = {Association {Between} {HIV} {Infection}, {Antiretroviral} {Therapy}, and {Risk} of {Acute} {Myocardial} {Infarction}: {A} {Cohort} and {Nested} {Case}–{Control} {Study} {Using} {Québecʼs} {Public} {Health} {Insurance} {Database}:},
	volume = {57},
	issn = {1525-4135},
	shorttitle = {Association {Between} {HIV} {Infection}, {Antiretroviral} {Therapy}, and {Risk} of {Acute} {Myocardial} {Infarction}},
	url = {http://journals.lww.com/00126334-201107010-00011},
	doi = {10.1097/QAI.0b013e31821d33a5},
	language = {en},
	number = {3},
	urldate = {2020-11-18},
	journal = {JAIDS Journal of Acquired Immune Deficiency Syndromes},
	author = {Durand, Madeleine and Sheehy, Odile and Baril, Jean-Guy and Lelorier, Jacques and Tremblay, Cécile L},
	month = jul,
	year = {2011},
	pages = {245--253},
}

@article{deeks_hiv_2011,
	title = {{HIV} {Infection}, {Inflammation}, {Immunosenescence}, and {Aging}},
	volume = {62},
	issn = {0066-4219, 1545-326X},
	url = {http://www.annualreviews.org/doi/10.1146/annurev-med-042909-093756},
	doi = {10.1146/annurev-med-042909-093756},
	language = {en},
	number = {1},
	urldate = {2020-11-18},
	journal = {Annual Review of Medicine},
	author = {Deeks, Steven G.},
	month = feb,
	year = {2011},
	pages = {141--155},
}

@article{neuhaus_risk_2010,
	title = {Risk of all-cause mortality associated with nonfatal {AIDS} and serious non-{AIDS} events among adults infected with {HIV}:},
	volume = {24},
	issn = {0269-9370},
	shorttitle = {Risk of all-cause mortality associated with nonfatal {AIDS} and serious non-{AIDS} events among adults infected with {HIV}},
	url = {http://journals.lww.com/00002030-201003130-00009},
	doi = {10.1097/QAD.0b013e3283365356},
	language = {en},
	number = {5},
	urldate = {2020-11-18},
	journal = {AIDS},
	author = {Neuhaus, Jacqueline and Angus, Brian and Kowalska, Justyna D and Rosa, Alberto La and Sampson, Jim and Wentworth, Deborah and Mocroft, Amanda},
	month = mar,
	year = {2010},
	pages = {697--706},
}

@article{lang_increased_2010,
	title = {Increased risk of myocardial infarction in {HIV}-infected patients in {France}, relative to the general population:},
	volume = {24},
	issn = {0269-9370},
	shorttitle = {Increased risk of myocardial infarction in {HIV}-infected patients in {France}, relative to the general population},
	url = {http://journals.lww.com/00002030-201005150-00021},
	doi = {10.1097/QAD.0b013e328339192f},
	language = {en},
	number = {8},
	urldate = {2020-11-18},
	journal = {AIDS},
	author = {Lang, Sylvie and Mary-Krause, Murielle and Cotte, Laurent and Gilquin, Jacques and Partisani, Marialuisa and Simon, Anne and Boccara, Franck and Bingham, Annie and Costagliola, Dominique},
	month = may,
	year = {2010},
	pages = {1228--1230},
}

@article{noauthor_causes_2010,
	title = {Causes of {Death} in {HIV}‐1–{Infected} {Patients} {Treated} with {Antiretroviral} {Therapy}, 1996–2006: {Collaborative} {Analysis} of 13 {HIV} {Cohort} {Studies}},
	volume = {50},
	issn = {1058-4838, 1537-6591},
	shorttitle = {Causes of {Death} in {HIV}‐1–{Infected} {Patients} {Treated} with {Antiretroviral} {Therapy}, 1996–2006},
	url = {https://academic.oup.com/cid/article-lookup/doi/10.1086/652283},
	doi = {10.1086/652283},
	language = {en},
	number = {10},
	urldate = {2020-11-18},
	journal = {Clinical Infectious Diseases},
	month = may,
	year = {2010},
	pages = {1387--1396},
}

@article{terzian_factors_2009,
	title = {Factors {Associated} with {Preclinical} {Disability} and {Frailty} among {HIV}-{Infected} and {HIV}-{Uninfected} {Women} in the {Era} of {cART}},
	volume = {18},
	issn = {1540-9996, 1931-843X},
	url = {http://www.liebertpub.com/doi/10.1089/jwh.2008.1090},
	doi = {10.1089/jwh.2008.1090},
	language = {en},
	number = {12},
	urldate = {2020-11-18},
	journal = {Journal of Women's Health},
	author = {Terzian, Arpi S. and Holman, Susan and Nathwani, Niyati and Robison, Esther and Weber, Kathleen and Young, Mary and Greenblatt, Ruth M. and Gange, Stephen J.},
	month = dec,
	year = {2009},
	pages = {1965--1974},
}

@article{onen_frailty_2009,
	title = {Frailty among {HIV}-infected persons in an urban outpatient care setting},
	volume = {59},
	issn = {01634453},
	url = {https://linkinghub.elsevier.com/retrieve/pii/S0163445309002369},
	doi = {10.1016/j.jinf.2009.08.008},
	language = {en},
	number = {5},
	urldate = {2020-11-18},
	journal = {Journal of Infection},
	author = {Önen, Nur F. and Agbebi, Abayomi and Shacham, Enbal and Stamm, Kate E. and Önen, Alev R. and Overton, E. Turner},
	month = nov,
	year = {2009},
	pages = {346--352},
}

@article{masel_frailty_2009,
	title = {Frailty and health related quality of life in older {Mexican} {Americans}},
	volume = {7},
	issn = {1477-7525},
	url = {https://hqlo.biomedcentral.com/articles/10.1186/1477-7525-7-70},
	doi = {10.1186/1477-7525-7-70},
	language = {en},
	number = {1},
	urldate = {2020-11-18},
	journal = {Health and Quality of Life Outcomes},
	author = {Masel, Meredith C and Graham, James E and Reistetter, Timothy A and Markides, Kyriakos S and Ottenbacher, Kenneth J},
	month = dec,
	year = {2009},
	pages = {70},
}

@article{effros_aging_2008,
	title = {Aging and {Infectious} {Diseases}: {Workshop} on {HIV} {Infection} and {Aging}: {What} {Is} {Known} and {Future} {Research} {Directions}},
	volume = {47},
	issn = {1058-4838, 1537-6591},
	shorttitle = {Aging and {Infectious} {Diseases}},
	url = {https://academic.oup.com/cid/article-lookup/doi/10.1086/590150},
	doi = {10.1086/590150},
	language = {en},
	number = {4},
	urldate = {2020-11-18},
	journal = {Clinical Infectious Diseases},
	author = {Effros, Rita B. and Fletcher, Courtney V. and Gebo, Kelly and Halter, Jeffrey B. and Hazzard, William R. and Horne, Frances McFarland and Huebner, Robin E. and Janoff, Edward N. and Justice, Amy C. and Kuritzkes, Daniel and Nayfield, Susan G. and Plaeger, Susan F. and Schmader, Kenneth E. and Ashworth, John R. and Campanelli, Christine and Clayton, Charles P. and Rada, Beth and Woolard, Nancy F. and High, Kevin P.},
	month = aug,
	year = {2008},
	pages = {542--553},
}

@article{currier_epidemiological_2008,
	title = {Epidemiological {Evidence} for {Cardiovascular} {Disease} in {HIV}-{Infected} {Patients} and {Relationship} to {Highly} {Active} {Antiretroviral} {Therapy}},
	volume = {118},
	issn = {0009-7322, 1524-4539},
	url = {https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.107.189624},
	doi = {10.1161/CIRCULATIONAHA.107.189624},
	language = {en},
	number = {2},
	urldate = {2020-11-18},
	journal = {Circulation},
	author = {Currier, Judith S. and Lundgren, Jens D. and Carr, Andrew and Klein, Daniel and Sabin, Caroline A. and Sax, Paul E. and Schouten, Jeffrey T. and Smieja, Marek and {for Working Group 2}},
	month = jul,
	year = {2008},
}

@article{triant_increased_2007,
	title = {Increased {Acute} {Myocardial} {Infarction} {Rates} and {Cardiovascular} {Risk} {Factors} among {Patients} with {Human} {Immunodeficiency} {Virus} {Disease}},
	volume = {92},
	issn = {0021-972X, 1945-7197},
	url = {https://academic.oup.com/jcem/article/92/7/2506/2598256},
	doi = {10.1210/jc.2006-2190},
	abstract = {Abstract 
            Context: Metabolic changes and smoking are common among HIV patients and may confer increased cardiovascular risk. 
            Objective: The aim of the study was to determine acute myocardial infarction (AMI) rates and cardiovascular risk factors in HIV compared with non-HIV patients in two tertiary care hospitals. 
            Design, Setting, and Participants: We conducted a health care system-based cohort study using a large data registry with 3,851 HIV and 1,044,589 non-HIV patients. AMI rates were determined among patients receiving longitudinal care between October 1, 1996, and June 30, 2004. 
            Main Outcome Measures: The primary outcome was myocardial infarction, identified by International Classification of Diseases coding criteria. 
            Results: AMI was identified in 189 HIV and 26,142 non-HIV patients. AMI rates per 1000 person-years were increased in HIV vs. non-HIV patients [11.13 (95\% confidence interval [CI] 9.58–12.68) vs. 6.98 (95\% CI 6.89–7.06)]. The HIV cohort had significantly higher proportions of hypertension (21.2 vs. 15.9\%), diabetes (11.5 vs. 6.6\%), and dyslipidemia (23.3 vs. 17.6\%) than the non-HIV cohort (P \< 0.0001 for each comparison). The difference in AMI rates between HIV and non-HIV patients was significant, with a relative risk (RR) of 1.75 (95\% CI 1.51–2.02; P \< 0.0001), adjusting for age, gender, race, hypertension, diabetes, and dyslipidemia. In gender-stratified models, the unadjusted AMI rates per 1000 person-years were higher for HIV patients among women (12.71 vs. 4.88 for HIV compared with non-HIV women), but not among men (10.48 vs. 11.44 for HIV compared with non-HIV men). The RRs (for HIV vs. non-HIV) were 2.98 (95\% CI 2.33–3.75; P \< 0.0001) for women and 1.40 (95\% CI 1.16–1.67; P = 0.0003) for men, adjusting for age, gender, race, hypertension, diabetes, and dyslipidemia. A limitation of this database is that it contains incomplete data on smoking. Smoking could not be included in the overall regression model, and some of the increased risk may be accounted for by differences in smoking rates. 
            Conclusions: AMI rates and cardiovascular risk factors were increased in HIV compared with non-HIV patients, particularly among women. Cardiac risk modification strategies are important for the long-term care of HIV patients.},
	language = {en},
	number = {7},
	urldate = {2020-11-18},
	journal = {The Journal of Clinical Endocrinology \& Metabolism},
	author = {Triant, Virginia A. and Lee, Hang and Hadigan, Colleen and Grinspoon, Steven K.},
	month = jul,
	year = {2007},
	pages = {2506--2512},
}

Abstract Context: Metabolic changes and smoking are common among HIV patients and may confer increased cardiovascular risk. Objective: The aim of the study was to determine acute myocardial infarction (AMI) rates and cardiovascular risk factors in HIV compared with non-HIV patients in two tertiary care hospitals. Design, Setting, and Participants: We conducted a health care system-based cohort study using a large data registry with 3,851 HIV and 1,044,589 non-HIV patients. AMI rates were determined among patients receiving longitudinal care between October 1, 1996, and June 30, 2004. Main Outcome Measures: The primary outcome was myocardial infarction, identified by International Classification of Diseases coding criteria. Results: AMI was identified in 189 HIV and 26,142 non-HIV patients. AMI rates per 1000 person-years were increased in HIV vs. non-HIV patients [11.13 (95% confidence interval [CI] 9.58–12.68) vs. 6.98 (95% CI 6.89–7.06)]. The HIV cohort had significantly higher proportions of hypertension (21.2 vs. 15.9%), diabetes (11.5 vs. 6.6%), and dyslipidemia (23.3 vs. 17.6%) than the non-HIV cohort (P < 0.0001 for each comparison). The difference in AMI rates between HIV and non-HIV patients was significant, with a relative risk (RR) of 1.75 (95% CI 1.51–2.02; P < 0.0001), adjusting for age, gender, race, hypertension, diabetes, and dyslipidemia. In gender-stratified models, the unadjusted AMI rates per 1000 person-years were higher for HIV patients among women (12.71 vs. 4.88 for HIV compared with non-HIV women), but not among men (10.48 vs. 11.44 for HIV compared with non-HIV men). The RRs (for HIV vs. non-HIV) were 2.98 (95% CI 2.33–3.75; P < 0.0001) for women and 1.40 (95% CI 1.16–1.67; P = 0.0003) for men, adjusting for age, gender, race, hypertension, diabetes, and dyslipidemia. A limitation of this database is that it contains incomplete data on smoking. Smoking could not be included in the overall regression model, and some of the increased risk may be accounted for by differences in smoking rates. Conclusions: AMI rates and cardiovascular risk factors were increased in HIV compared with non-HIV patients, particularly among women. Cardiac risk modification strategies are important for the long-term care of HIV patients.

@article{goulet_patterns_2007,
	title = {Do {Patterns} of {Comorbidity} {Vary} by {HIV} {Status}, {Age}, and {HIV} {Severity}?},
	volume = {45},
	issn = {1058-4838, 1537-6591},
	url = {https://academic.oup.com/cid/article-lookup/doi/10.1086/523577},
	doi = {10.1086/523577},
	language = {en},
	number = {12},
	urldate = {2020-11-18},
	journal = {Clinical Infectious Diseases},
	author = {Goulet, J. L. and Fultz, S. L. and Rimland, D. and Butt, A. and Gibert, C. and Rodriguez-Barradas, M. and Bryant, K. and Justice, A. C.},
	month = dec,
	year = {2007},
	pages = {1593--1601},
}

@article{high_hiv_2006,
	title = {{HIV} {Infection} and {Dementia} in {Older} {Adults}},
	volume = {42},
	issn = {1058-4838, 1537-6591},
	url = {https://academic.oup.com/cid/article-lookup/doi/10.1086/503565},
	doi = {10.1086/503565},
	language = {en},
	number = {10},
	urldate = {2020-11-18},
	journal = {Clinical Infectious Diseases},
	author = {High, K. P. and Valcour, V. and Paul, R.},
	month = may,
	year = {2006},
	pages = {1449--1454},
}

@article{rusch_no_2004,
	title = {[{No} title found]},
	volume = {2},
	issn = {14777525},
	url = {http://hqlo.biomedcentral.com/articles/10.1186/1477-7525-2-46},
	doi = {10.1186/1477-7525-2-46},
	number = {1},
	urldate = {2020-11-18},
	journal = {Health and Quality of Life Outcomes},
	author = {Rusch, Melanie and Nixon, Stephanie and Schilder, Arn and Braitstein, Paula and Chan, Keith and Hogg, Robert S},
	year = {2004},
	pages = {46},
}

@article{murphy_highly_2001,
	title = {Highly {Active} {Antiretroviral} {Therapy} {Decreases} {Mortality} and {Morbidity} in {Patients} with {Advanced} {HIV} {Disease}},
	volume = {135},
	issn = {0003-4819},
	url = {http://annals.org/article.aspx?doi=10.7326/0003-4819-135-1-200107030-00005},
	doi = {10.7326/0003-4819-135-1-200107030-00005},
	language = {en},
	number = {1},
	urldate = {2020-11-18},
	journal = {Annals of Internal Medicine},
	author = {Murphy, Edward L. and Collier, Ann C. and Kalish, Leslie A. and Assmann, Susan F. and Para, Michael F. and Flanigan, Timothy P. and Kumar, Princy N. and Mintz, Letty and Wallach, Frances R. and Nemo, George J. and {for the Viral Activation Transfusion Study Investigators*}},
	month = jul,
	year = {2001},
	pages = {17},
}

@article{palella_declining_1998,
	title = {Declining {Morbidity} and {Mortality} among {Patients} with {Advanced} {Human} {Immunodeficiency} {Virus} {Infection}},
	volume = {338},
	issn = {0028-4793, 1533-4406},
	url = {http://www.nejm.org/doi/abs/10.1056/NEJM199803263381301},
	doi = {10.1056/NEJM199803263381301},
	language = {en},
	number = {13},
	urldate = {2020-11-18},
	journal = {New England Journal of Medicine},
	author = {Palella, Frank J. and Delaney, Kathleen M. and Moorman, Anne C. and Loveless, Mark O. and Fuhrer, Jack and Satten, Glen A. and Aschman, Diane J. and Holmberg, Scott D.},
	month = mar,
	year = {1998},
	pages = {853--860},
}