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Department of Medicine, University of Colorado Health Sciences Center, Denver, CO 80262
An in vitro proliferative defect has been observed in HIV-1-specific CD4+ T cells from infected subjects with high-level plasma HIV-1 viremia. To determine the mechanism of this defect, HIV-1 Gag-specific CD4+ T cells from treated and untreated HIV-1-infected subjects were analyzed for cytokine profile, proliferative capacity, and maturation state. Unexpectedly high frequencies of HIV-1-specific, IL-2-producing CD4+ T cells were measured in subjects with low or undetectable plasma HIV-1 loads, regardless of treatment status, and IL-2 frequencies correlated inversely with viral loads. IL-2-producing CD4+ T cells also primarily displayed a central memory (TCm; CCR7+CD45RA-) maturation phenotype, whereas IFN-
-producing cells were mostly effector memory (TEm, CCR7-CD45RA-). Among Gag-specific, IFN--producing CD4+ T cells, higher TEm frequencies and lower TCm frequencies were observed in untreated, high viral load subjects than in subjects with low viral loads. The percentage of HIV-1 Gag-specific CD4+ TCm correlated inversely with HIV-1 viral load and directly with Gag-specific CD4+ T cell proliferation, whereas the opposite relationships were observed for HIV-1-specific CD4+ TEm. These results suggest that HIV-1 viremia skews Gag-specific CD4+ T cells away from an IL-2-producing TCm phenotype and toward a poorly proliferating TEm phenotype, which may limit the effectiveness of the HIV-1-specific immune response.
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