This study shows that HAART may increase the survival, clinical status and radiological features of AIDS patients with PML. Clearance of JC virus from CSF has been found, suggesting that immune reconstitution can interrupt the JC virus lytic cycle.

HIV-infected patients aged ≥55 years have a high prevalence of frailty and a high burden of functional impairment. Optimal management of this population requires close collaboration between infectious diseases specialists and geriatricians.

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People living with HIV-1 experience an accelerated aging due to the persistent and chronic activation of the immune system. This phenomenon conduces to immune exhaustion and precipitate immunosenescence. In general, frailty is defined as a syndrome of physiological degeneration in the elderly. Circulating naïve and memory T cells were studied by flow cytometry in non-frail and frail HIV-1-infected groups. Thymopoiesis, cell activation, senescence and cell proliferation were analyzed by CD31, HLA-DR/CD38, CD28/CD57 and Ki-67 expression, respectively. Plasma levels of sCD14 and MDA were measured by ELISA. Frail infected individuals showed a reduced number of memory T cells, both CD4 + and CD8 + populations. Activated CD3 + CD4 + HLA-DR + T cells were lower in frail individuals, and directly correlated with CD3 + CD8 + HLA-DR + and CD8 M cells. Senescent CD8 + CD28 − CD57 + cells were reduced in frail HIV-1 infected individuals and inversely correlated with CD8 RTE , CD8 N and CD3 + CD4 + HLA-DR +. Higher plasma levels of sCD14 and MDA were found in HIV-1 infected frail individuals. Our data show association among frailty, markers of immune activation and oxidative stress. Understanding the immune mechanisms underlying frailty status in HIV-1 population is of high relevance not only for the prediction of continuing longevity but also for the identification of potential strategies for the elderly.

Incomplete immune reconstitution and persistent immune system hyperactivation in spite of highly active antiretroviral therapy continue to be a challenge. Both facts may lead to an increased risk for AIDS-defining and non AIDS-defining clinical conditions and may also promote atherogenesis and liver fibrogenesis in HIV and hepatitis C virus-coinfected patients. In this article, the use of new markers to assess immune reconstitution and immune activation and the incidence and clinical consequences of immunediscordant response to antiretroviral therapy are addressed. Likewise, the impact of immune dysfunction on atherogenesis and liver fibrogenesis are reviewed. Finally, it is discussed whether therapy with drugs belonging to the family of CCR5 inhibitors may provide additional immunological benefit in HIV-infected patients. J o ur nal o f A ID S & Cli n ic a l R es earc h