Journal
ANNUAL REVIEW OF MEDICINE, VOL 62, 2011
Volume 62, Issue -, Pages 141-155Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev-med-042909-093756
Keywords
CMV; CD28; CD38; frailty; telomere
Categories
Funding
- NATIONAL CENTER FOR RESEARCH RESOURCES [UL1RR024131] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL095130] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI087145, P01AI071713, P30AI027763, K24AI069994, R24AI067039] Funding Source: NIH RePORTER
- NCRR NIH HHS [UL1 RR024131] Funding Source: Medline
- NHLBI NIH HHS [R01HL095130, R01 HL095130] Funding Source: Medline
- NIAID NIH HHS [R24 AI067039, R01 AI087145, P30 AI027763, K24AI069994, P01 AI071713, P0 AI27763, K24 AI069994, P01AI071713, 1 R24 AI067039-1] Funding Source: Medline
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Although antiretroviral therapy for HIV infection prevents AIDS-related complications and prolongs life, it does not fully restore health. Long-term treated patients remain at higher than expected risk for a number of complications typically associated with aging, including cardiovascular disease, cancer, osteoporosis, and other end-organ diseases. The potential effect of HIV on health is perhaps most clearly exhibited by a number of immunologic abnormalities that persist despite effective suppression of HIV replication. These changes are consistent with some of the changes to the adaptive immune system that are seen in the very old (immunosenescence) and that are likely related in part to persistent inflammation. HIV-associated inflammation and immunosenescence have been implicated as causally related to the premature onset of other end-organ diseases. Novel therapeutic strategies aimed at preventing or reversing these immunologic defects may be necessary if HIV-infected patients are to achieve normal life span.
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