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Murine T cells potently restrict human immunodeficiency virus infection

  1. Author:
    Baumann, J. G.
    Unutmaz, D.
    Miller, M. D.
    Breun, S. K. J.
    Grill, S. M.
    Mirro, J.
    Littman, D. R.
    Rein, A.
    KewalRamani, V. N.
  2. Author Address

    NCI, Frederick Canc Res & Dev Ctr, HIV Drug Resistance Program, Frederick, MD 21702 USA. Vanderbilt Univ, Sch Med, Dept Microbiol & Immunol, Nashville, TN 37212 USA. Merck Res Labs, Dept Biol Chem, W Point, PA USA. NYU, Sch Med, Howard Hughes Med Inst, New York, NY USA. NYU, Sch Med, Skirball Inst Biomol Med, New York, NY USA KewalRamani, VN, NCI, Frederick Canc Res & Dev Ctr, HIV Drug Resistance Program, Bldg 535,Rm 123, Frederick, MD 21702 USA
    1. Year: 2004
    2. Date: NOV
  1. Journal: Journal of Virology
    1. 78
    2. 22
    3. Pages: 12537-12547
  2. Type of Article: Article
  1. Abstract:

    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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External Sources

  1. WOS: 000224781400046

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