Heightened T-cell proliferation without an elevation of CD4+ T cell spontaneous apoptosis in AIDS patients.

T lymphocyte turnover has been studied extensively in HIV infection. The dynamic characteristics of various subsets of T cells in antiretroviral-naive, HIV-1-infected individuals, however, have not been well defined. Here, we performed a cross-sectional study using peripheral blood T cells from 39 antiretroviral-naive, chronically HIV-infected patients, as well as 16 healthy, HIV-negative controls. T-cell subset turnover rates were measured by Ki-67 antigen staining; levels of spontaneous apoptosis and activation in T-cell subsets were also determined by flow cytometry. Surprisingly, with disease progression, the level of T-cell spontaneous apoptosis did not increase significantly, despite a heightened rate of T-cell subset turnover and increased expression of the CD38 activation marker. These data refute the idea that increased T cell turnover is merely a homeostatic process in response to CD4 T cell loss during HIV disease progression, and suggest that future mechanistic studies may be needed for a comprehensive understanding of T-cell dynamics during HIV infection. Such understanding may help to develop new strategies for the immune modulation of clinical disease.