期刊
JOURNAL OF VIROLOGY
卷 78, 期 22, 页码 12537-12547出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.78.22.12537-12547.2004
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资金
- NIAID NIH HHS [R01 AI033856, AI 36606, R01 AI049131, AI 33856, AI 49131] Funding Source: Medline
Development of a mouse model for human immunodeficiency virus type 1 (HIV-1) infection has advanced through the progressive identification of host cell factors required for HIV-1 replication. Murine cells lack HIV-1 receptor molecules, do not support efficient viral gene expression, and lack factors necessary for the assembly and release of virions. Many of these blocks have been described using mouse fibroblast cell lines. Here we identify a postentry block to HIV-1 infection in mouse T-cell lines that has not been detected in mouse fibroblasts. While murine fibroblastic lines are comparable to human T-cell lines in permissivity to HIV-1 transduction, infection of marine T cells is 100-fold less efficient. Virus entry occurs efficiently in marine T cells. However, reduced efficiency of the completion of reverse transcription and nuclear transfer of the viral preintegration complex are observed. Although this block has similarities to the restriction of murine retroviruses by Fv1, there is no correlation of HIV-1 susceptibility with cellular Fv1 genotypes. In addition, the block to HIV-1 infection in marine T-cell lines cannot be saturated by a high virus dose. Further studies of this newly identified block may lend insight into the early events of retroviral replication and reveal new targets for antiretroviral interventions.
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