Article

The Role of Cellular Factors in Promoting HIV Budding

Program in Gene Function and Expression, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Journal of Molecular Biology (Impact Factor: 4.33). 07/2011; 410(4):525-33. DOI: 10.1016/j.jmb.2011.04.055
Source: PubMed

ABSTRACT Human immunodeficiency virus type 1 (HIV-1) becomes enveloped while budding through the plasma membrane, and the release of nascent virions requires a membrane fission event that separates the viral envelope from the cell surface. To facilitate this crucial step in its life cycle, HIV-1 exploits a complex cellular membrane remodeling and fission machinery known as the endosomal sorting complex required for transport (ESCRT) pathway. HIV-1 Gag directly interacts with early-acting components of this pathway, which ultimately triggers the assembly of the ESCRT-III membrane fission complex at viral budding sites. Surprisingly, HIV-1 requires only a subset of ESCRT-III components, indicating that the membrane fission reaction that occurs during HIV-1 budding differs in crucial aspects from topologically related cellular abscission events.

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Available from: Heinrich G Gottlinger, Aug 25, 2015
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    • "The myristylation of Gly2 in MA targets the Gag protein to the plasma membrane [1] [20], and mutation of this glycine myristylation site prevents virus budding and leads to accumulation of Gag within the host cell [21]. The structure of MA has been determined by both X-ray crystallography and NMR, and comprises 5 alpha helices and a three strand mixed beta sheet [22] [23] [24] which forms a trimer in the virion shell in the mature HIV-1 particle. "
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