title: How to engage Cofilin.
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.
authors.affiliation: George Washington University, Department of Microbiology, Immunology and Tropical Medicine, Washington, DC 20037, USA. mtmmib@gwumc.edu
authors.forename: Michael
authors.initials: M
authors.lastname: Bukrinsky
mesh_terms: D015496:CD4-Positive T-Lymphocytes / Q000821:virology*; D051338:Cofilin 1 / Q000378:metabolism*; D006678:HIV / Q000502:physiology*; D006801:Humans; D015398:Signal Transduction; D053586:Virus Internalization
chemical_list: D051338:Cofilin 1