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CUTTING EDGE |
*
Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD;
Intramural Research Support Program-Scientific Applications International Corporation, Frederick, Laboratory of Molecular Immunoregulation, National Cancer Institute, Frederick Cancer Research and Development Center, Frederick, MD;
HIV Unit, Wilford Hall Medical Center, Lackland Air Force Base, TX.
HIV-1 infection is accompanied by qualitative and quantitative
defects in CD4+ T lymphocytes. Loss of immune
function in HIV patients is usually associated with a profound
dysregulation of cytokine production. To investigate whether cytokine
signaling defects occur during HIV infection, PHA blasts from healthy
human donors were infected with two strains of HIV-1 and screened for
the expression of STAT proteins used in cytokine signaling. A selective
decrease in STAT5B was seen 8 days after infection with the BZ167
dual-tropic HIV isolate, but not with the Ba-L, M-tropic strain. Based
on these findings, purified T cells from HIV-infected patients in
different stages of disease were also tested for STAT expression;
decreases in STAT5A, STAT5B, and STAT1
were observed in all
patients. The reduction in STATs seen in vivo and in vitro after HIV
infection may contribute to the loss of T cell function in HIV disease.
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