HIV Infection as a Model of Accelerated Immunosenescence
Since its discovery in 1983, HIV-1 has become the most extensively studied pathogen in history. Massive CD4+ T-cell depletion and sustained immune activation and inflammation are hallmarks of HIV-1 infection. However, many insights underlying the onset of immunodeficiency that develops during HIV-1 infection remain to be resolved. In recent years, an intriguing parallel between HIV-1 infection and aging has emerged: many of the alterations that affect innate and adaptive immune cell compartments in HIV-infected patients are reminiscent of the process of immune aging, characteristic of old age. These alterations, of which the alleged cause is the systemic chronic immune activation established in patients, likely participate to the decline of immune competence with HIV disease progression. Of note, the comparison between HIV-1-infected patients and uninfected elderly adults goes beyond the sole onset of immunosenescence and extends to the deterioration of a number of physiological functions related to inflammation and systemic aging. Our understanding of the precise link between immune activation and aging in HIV-1 infection is complicated by the influence of coinfections and lifestyle factors. Developing rational interventions to reduce the hyper-inflammatory status and age resembling manifestations in HIV-1-infected patients are major goals of the HIV community.
KeywordsHIV pathogenesis CD4+ T cells Immune activation Regenerative capacity Exhaustion
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