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.

Cellular Senescence, Immunosenescence and HIV / Fulop, T.; Herbein, G.; Cossarizza, A.; Witkowski, J. M.; Frost, E.; Dupuis, G.; Pawelec, G.; Larbi, A.. - 42:(2016), pp. 28-46. [10.1159/000448542]

Cellular Senescence, Immunosenescence and HIV

Cossarizza A.;
2016

Abstract

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.
2016
HIV and Aging
Cellular Senescence, Immunosenescence and HIV / Fulop, T.; Herbein, G.; Cossarizza, A.; Witkowski, J. M.; Frost, E.; Dupuis, G.; Pawelec, G.; Larbi, A.. - 42:(2016), pp. 28-46. [10.1159/000448542]
Fulop, T.; Herbein, G.; Cossarizza, A.; Witkowski, J. M.; Frost, E.; Dupuis, G.; Pawelec, G.; Larbi, A.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11380/1229239
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