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Open Access Highly Accessed Review

The trinity of the cortical actin in the initiation of HIV-1 infection

Mark Spear, Jia Guo and Yuntao Wu*

Author Affiliations

National Center for Biodefense and Infectious Diseases, Department of Molecular and Microbiology, George Mason University, Manassas, VA, 20110, USA

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Retrovirology 2012, 9:45  doi:10.1186/1742-4690-9-45

Published: 28 May 2012

Abstract

For an infecting viral pathogen, the actin cortex inside the host cell is the first line of intracellular components that it encounters. Viruses devise various strategies to actively engage or circumvent the actin structure. In this regard, the human immunodeficiency virus-1 (HIV-1) exemplifies command of cellular processes to take control of actin dynamics for the initiation of infection. It has becomes increasingly evident that cortical actin presents itself both as a barrier to viral intracellular migration and as a necessary cofactor that the virus must actively engage, particularly, in the infection of resting CD4 blood T cells, the primary targets of HIV-1. The coercion of this most fundamental cellular component permits infection by facilitating entry, reverse transcription, and nuclear migration, three essential processes for the establishment of viral infection and latency in blood T cells. It is the purpose of this review to examine, in detail, the manifestation of viral dependence on the actin cytoskeleton, and present a model of how HIV utilizes actin dynamics to initiate infection.

Keywords:
HIV-1; gp120; Nef; Actin; Cofilin; LIMK1; Arp2/3; CD4; CXCR4; Chemokine; Chemotaxis