The percentage of people living with HIV/AIDS in USA who are over 50 years old is on the rise (Figure 2), and it is estimated that, by 2015, people over 50 will constitute the majority of all people living with HIV/AIDS in USA.5 Figure 1 Estimated survival of 25-year-old HIV-infected and non-infected men in Denmark, 1995–2005. Figure 2 Estimated percentage of persons living with HIV/AIDS in USA who are older than 50, by year, 2001–2007. As a result, we are encountering more chronic diseases typical of aging: cardiovascular
disease, diabetes mellitus, dyslipidemia, osteoporosis and bone fractures, Inhibitors,research,lifescience,medical malignancies, and neurocognitive impairment.6 In addition, the accelerated aging of the immune
system of HIV carriers has been demonstrated,7 and this is accompanied by the parallel process of increased incidence of chronic diseases typical of aging and early signs of physical and functional frailty in this population.8 Accelerated aging may be a result of several factors, including HIV infection Inhibitors,research,lifescience,medical itself, ART side-effects, and the aging of the immune system. It is now clear that the function of the immune system declines with age, but is the decline affecting Inhibitors,research,lifescience,medical the accelerated aging in HIV patients? These evolving processes which interact with each other are becoming a major factor in treatment decisions of HIV carriers and shape research and clinical priorities, and they will be discussed further in this review. IMMUNOSENESCENCE AND HIV INFECTION Physiological aging of the immune system, termed immune senescence, is associated with Inhibitors,research,lifescience,medical a dysfunction in innate and selleckchem adaptive immunity which diminishes the ability to respond to novel foreign antigens—vaccinations and infections. Inhibitors,research,lifescience,medical Similar changes in immune functions occur in people with chronic HIV infection but at a much younger age. Changes seen in adaptive immune system manifest as lower naïve:memory CD4 ratio and enrichment of CD28−/CD57+/CD8+ effector T cells.9 The latter are senescent cells with shorter telomeres and limited proliferative capacity. In addition, there are putative qualitative and quantitative changes
in T regulatory cells10 and a decrease in the diversity of naïve B cells and a qualitative Resveratrol B cell dysfunction.11 In HIV carriers, peripheral blood lymphocytes show a tendency towards T cell senescence with enrichment of CD28−/CD57+/CD8+ T cells and inverted ratio of naïve/memory T cells,9 as seen in normal aging. However, the immunophenotypic changes seen in HIV-infected patients, though similar to the changes seen in HIV-negative individuals, appear 20–30 years earlier.12 Considering the innate immune system, peripheral blood monocytes from young HIV-positive individuals exhibit changes in phenotype, function, and telomere length that closely resemble those observed in elderly controls aged approximately 30 years older.