Current HIV/AIDS Reports

, Volume 7, Issue 1, pp 4–10

Early Immune Senescence in HIV Disease


DOI: 10.1007/s11904-009-0038-4

Cite this article as:
Desai, S. & Landay, A. Curr HIV/AIDS Rep (2010) 7: 4. doi:10.1007/s11904-009-0038-4


Non-AIDS-defining co-morbidities that occur despite viral suppression and immune reconstitution using antiretroviral therapy depict early aging process in HIV-infected individuals. During aging, a reduction in T-cell renewal, together with a progressive enrichment of terminally differentiated T cells, translates into a general decline of the immune system, gradually leading to immunosenescence. Inflammation is a hallmark of age-associated comorbidities, and immune activation is a hallmark of HIV disease. Constant stimulation of the immune system by HIV or due to co-infections activates the innate and adaptive immune system, resulting in release of mediators of inflammation. Immune activation coupled with lack of anti-inflammatory responses likely results in accelerated aging in HIV disease. Dysfunctional thymic output, along with HIV-mediated disruption of the gastrointestinal barrier leading to microbial translocation, contributes to the circulating antigenic load driving early senescence in HIV disease.


SenesceneActivationInflammationMicrobial translocation

Copyright information

© Springer Science+Business Media, LLC 2010

Authors and Affiliations

  1. 1.Department of Immunology/MicrobiologyRush University Medical CenterChicagoUSA