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.
journal_name
Retrovirologyjournal_title
Retrovirologyauthors
Bukrinsky Mdoi
10.1186/1742-4690-5-85subject
Has Abstractpub_date
2008-09-22 00:00:00pages
85issn
1742-4690pii
1742-4690-5-85journal_volume
5pub_type
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