Cellular Senescence, Immunosenescence and HIV

Nov 23, 2016Interdisciplinary topics in gerontology and geriatrics

Aging of Cells and the Immune System in HIV

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Abstract

Aging is associated with immunosenescence and low-grade inflammation, termed inflamm-aging.

Immunosenescence and inflamm-aging are linked to age-related diseases such as cardiovascular, neurodegenerative, metabolic diseases, and cancer.
Chronic viral infections, like cytomegalovirus, contribute to the process of inflamm-aging.
HIV infection has evolved from a deadly disease to a chronic inflammatory condition due to effective antiretroviral therapy.
The relationship between immunosenescence and HIV infection raises questions about whether HIV causes premature aging or if aging enhances susceptibility to HIV.
There are similarities in immune and inflammatory changes between normal aging and HIV infection, but their interactions remain poorly understood.

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Aging is a complex biological process that leads to several physiological changes. Among these changes, the most striking are those involving the innate and adaptive parts of the immune system. Furthermore, these changes are associated with a low-grade inflammation called inflamm-aging, which is the result of several lifelong antigenic stimulations, including chronic viral infections such as cytomegalovirus. Immunosenescence, concomitantly with inflamm-aging, is considered as the leading cause of age-related diseases including cardiovascular, neurodegenerative and metabolic diseases, and cancer. HIV infection, once considered a unique deadly infectious disease, has now become a chronic disease with efficacious highly active antiretroviral therapy. This signifies that the treatment transforms HIV infection from a chronic infection to a chronic inflammatory disease. Most people with HIV infection become aged, and older adults have been contracting HIV infection. Thus, there is a great interest to study HIV infection in relation to immunosenescence and inflamm-aging to determine whether immunosenescence contributes to HIV infection, or if HIV is causing immunosenescence and, as such, represents a premature immunosenescence and accelerated aging. Although there are many similarities in the immune and inflammatory changes and the occurrence of age-related chronic diseases between normal aging and HIV infection, the interaction between these processes is not well understood, and consequently the concept that HIV infection is an accelerated aging model is questioned. Future studies are needed to effectively answer this question for the better care of HIV-infected elderly patients.

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Cellular Senescence, Immunosenescence and HIV

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