1887

Abstract

Human immunodeficiency virus type 1 (HIV-1) establishes latent infection of a certain population of CD4 host cells which could be long-term reservoirs for HIV-1. The expression of viral genes in such long-term infected cells is strongly regulated by cellular status, such as the phase of the cell cycle or stage of cell differentiation. Here, viral gene expression in synchronized U1 cells, a monocytic cell clone latently infected with HIV-1, was characterized. The expression of HIV-1 antigens was detected exclusively at G/M phase in U1 cells, irrespective of phorbol myristate acetate (PMA) treatment. The induction of HIV-1 gene expression in PMA-treated cells was due to the recruitment of NF-B with DNA-binding activity at G/M phase. Activated NF-B was induced only by PMAtreatment during the late G to S, but not after entering G phase, indicating that the transcriptional factor(s) involved in viral gene expression is also largely regulated by the host cell cycle. In contrast, the enhancement of antigen expression by treatment with tumour necrosis factor-alpha (TNF-) was cell cycle-independent. In fact, NF-B was activated 2 h after TNF- treatment at all stages of the cell cycle. Thus, the mechanisms of HIV-1 activation from latency in U1 cells by PMA and TNF- treatment are different. The model system using U1 cells shown here may provide insight into the mechanisms responsible for HIV-1 gene expression from latency.

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1998-06-01
2022-05-25
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