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    Retrovirology. 2008 Sep 22;5:85.

    How to engage Cofilin.

    Source

    George Washington University, Department of Microbiology, Immunology and Tropical Medicine, Washington, DC 20037, USA. mtmmib@gwumc.edu

    Abstract

    In HIV-infected people, resting CD4+ T cells are the main reservoir of latent virus and the reason for the failure of drug therapy to cure HIV infection. Still, we do not have a complete understanding of the factors regulating HIV replication in these cells. A recent paper in Cell describes a new trick that the virus uses to infect resting T cells. Interaction between the viral gp120 and cellular HIV co-receptor, CXCR4, during viral entry initiates signaling that activates cofilin, the main regulator of actin polymerization. As a result of this activation, actin is depolymerized, thus destroying the natural barrier to HIV replication. I discuss implications of this study for our understanding of HIV biology and development of novel anti-HIV therapeutic approaches.

    PMID:
    18808680
    [PubMed - indexed for MEDLINE]
    PMCID: PMC2567344
    Free PMC Article

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