Pathogenic Mechanisms In HIV Disease

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Studies have demonstrated that intermittent infusions of the T cell derived cytokine IL-2 can lead to profound increases in the size of the CD4+ pool. An analysis of the IL-7/IL-7 receptor (CD127) system revealed that CD127 expression on T cells was low and remained low in HIV-infected patients despite antiretroviral or IL-2 therapy, reflecting persistent aberration in the subset composition of the T-cell pool. In another study, contrary to prior reports, treatment of helminthic infection did not lead to a decrease in levels of HIV replication indicating the complex nature of the relationships between HIV infection immune activation and secondary infections. In other work, a novel series of mutations were noted in a patient with high-level resistance to HIV protease inhibitors. These mutations involved changes in the binding site, the cleavage site and in areas controlling overall replication competence. Finally, the paradoxical ability of Actinomycin D to increase HIV replication was found to be due to the induction of IL-6.