Abstract
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.
Original language | English (US) |
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Pages (from-to) | 4-10 |
Number of pages | 7 |
Journal | Current HIV/AIDS Reports |
Volume | 7 |
Issue number | 1 |
DOIs | |
State | Published - Feb 2010 |
Externally published | Yes |
Keywords
- Activation
- Inflammation
- Microbial translocation
- Senescene
ASJC Scopus subject areas
- Virology
- Infectious Diseases