CD8(+) T-cell responses are an essential antiviral host defense in persistent viral infections, and their sustained effectiveness is thought to be critically dependent on CD4(+) T-helper cells. To determine the relationship between HIV-1-induced CD4(+) T-cell depletion and hepatitis C virus (HCV)-specific CD8(+) T-cell responses during viral persistence, we studied 103 persons positive for HCV, 74 coinfected with HIV-1. CD8(+) T-cell responses to the entire HCV polyprotein were determined by using an interferon-gamma enzyme-linked immunospot (ELISpot) assay.
View Article and Find Full Text PDFCD8 T-cell responses are thought to be crucial for control of viremia in human immunodeficiency virus (HIV) infection but ultimately fail to control viremia in most infected persons. Studies in acute infection have demonstrated strong CD8-mediated selection pressure and evolution of mutations conferring escape from recognition, but the ability of CD8 T-cell responses that persist in late-stage infection to recognize viruses present in vivo has not been determined. Therefore, we studied 24 subjects with advanced HIV disease (median viral load = 142,000 copies/ml; median CD4 count = 71/ micro l) and determined HIV-1-specific CD8 T-cell responses to all expressed viral proteins using overlapping peptides by gamma interferon Elispot assay.
View Article and Find Full Text PDFWe screened 651 human immunodeficiency virus (HIV)-1-infected subjects for hepatitis B surface antigen (HBsAg) and antibody to hepatitis B surface antigen (anti-HBs). Of a total of 387 subjects who tested negative for both HBsAg and anti-HBs, 142 underwent further testing for isolated presence of antibody to hepatitis B core antigen (anti-HBc). Of these 142 subjects, 60 (42%) tested positive for anti-HBc (isolated anti-HBc).
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