期刊
JOURNAL OF VIROLOGY
卷 81, 期 7, 页码 3477-3486出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.01552-06
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Changes in T-cell function are a hallmark of human immunodeficiency virus type 1 (HIV-1) infection, but the pathogenic mechanisms leading to these changes are unclear. We examined the gene expression profiles in ex vivo human CD4(+) and CD8(+) T cells from untreated HIV-1-infected individuals at different clinical stages and rates of disease progression. Profiles of pure CD4(+) and CD8(+) T-cell subsets from HIV-1-infected nonprogressors with controlled viremia were indistinguishable from those of individuals not infected with HIV-1. Similarly, no gene clusters could distinguish T cells from individuals with early infection from those seen in chronic progressive HIV-1 infection, whereas differences were observed between uninfected individuals or nonprogressors versus early or chronic progressors. In early and chronic HIV-1 infection, three characteristic gene expression signatures were observed. (i) CD4(+) and CD8(+) T cells showed increased expression of interferon-stimulated genes (ISGs). However, some ISGs, including CXCL9, CXCL10, and CXCL11, and the interieukin-15 alpha receptor were not upregulated. (ii) CD4(+) and CD8(+) T cells showed a cluster similar to that observed in thymocytes. (iii) More genes were differentially regulated in CD8(+) T cells than in CD4(+) T cells, including a cluster of genes downregulated exclusively in CD8(+) T cells. In conclusion, HIV-1 infection induces a persistent T-cell transcriptional profile, early in infection, characterized by a dramatic but potentially aberrant interferon response and a profile suggesting an active thymic output. These findings highlight the complexity of the host-virus relationship in HIV-1 infection.
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