The immune systems of patients with HIV infection are characterized by a decrease in the number of helper/inducer (CD4) T lymphocytes. In an effort to determine whether these decreases were secondary to decreased T cell production or increased T cell destruction, a series of studies were carried out in which rates of T cell turnover were studied using in vivo labeling of DNA and ex vivo measuremnt of ki67 expression. Levels of expression of ki67 werer found to correlate with the degree of CD4+ T cell recovery thus providing further suport to the hypotheseis that the expansisonsof CD4+ T cells seen following antiretroviral therapy are directly related to decreases in immune system activation. To better understand the nature of CD4+ T cell recovery following treatment of HIV infection, a series of studies were carried out to functionally characterize CD4+ memory (CD45+) using the marker CD62L (L-selectin). CD62L+ cells were found to have characteristics of central memory cells based upon patterns of proliferation, cytokine production and mRNA profiles while CD62L- cells were found to have characteristics of effector memory cells. In collaborative studies with the Laboratory of Molecular Microbiology we were able to demonstrate that deletions in the V2 region of SIV-HIV recombinant viruses were associated with an increase in macrophage tropism.
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