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Study reveals how a Rab protein controls HIV-1 replication

Rockefeller University Press

4-May-2015 - HIV-1 replication requires the coordinated movement of the virus's components toward the plasma membrane of an immune cell, where the virions are assembled and ultimately released. A study in The Journal of Cell Biology reveals how a Rab protein that controls intracellular trafficking supports HIV-1 assembly by promoting high levels of an important membrane lipid.

New HIV-1 particles assemble at specialized sites in the plasma membrane that are enriched in PIP 2 , a phospholipid component of the membrane that recruits a viral protein called Pr55 Gag (Gag) that directs HIV-1 assembly. Because certain cell secretion pathways have been suggested to be required for this process, University of Buenos Aires researcher Matías Ostrowski and colleagues investigated whether a role might be played by Rab27a, a protein that guides delivery of membrane-bound compartments called endosomes to the plasma membrane.

Ostrowski and colleagues found that viral replication was impaired in immune cells lacking Rab27a. These cells showed reduced levels of PIP 2 at the plasma membrane and thus failed to recruit Gag to form viral assembly sites. The researchers determined that Rab27a boosted PIP 2 production at the plasma membrane by controlling the endosomal delivery of an enzyme that is necessary for production of the phospholipid to the cell periphery.

Ostrowski believes that these results open a path to investigate whether manipulating endosomal traffic could be a new target for anti-HIV-1 therapies.

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Pereyra Gerber, P., et al. 2015. J. Cell Biol. doi:10.1083/jcb.201409082

About The Journal of Cell Biology

The Journal of Cell Biology (JCB) is published by The Rockefeller University Press. All editorial decisions on manuscripts submitted are made by active scientists in conjunction with our in-house scientific editors. JCB content is posted to PubMed Central, where it is available to the public for free six months after publication. Authors retain copyright of their published works, and third parties may reuse the content for non-commercial purposes under a creative commons license. For more information, please visit http://www.jcb.org.

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Source: http://www.eurekalert.org/pub_releases/2015-05/rup-srh043015.php


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