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Viruses 2010, 2(5), 1190-1194; doi:10.3390/v2051190

HIV Nuclear Entry: Clearing the Fog

Department of Microbiology and Immunology, Vanderbilt University School of Medicine, A 5301 Medical Center North, Nashville TN 37232-2363, USA
Author to whom correspondence should be addressed.
Received: 21 April 2010 / Revised: 5 May 2010 / Accepted: 5 May 2010 / Published: 11 May 2010
(This article belongs to the Section Editorial)
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HIV-1 and other lentiviruses have the unusual capability of infecting nondividing cells, but the mechanism by which they cross an intact nuclear membrane is mysterious. Recent work, including a new study (Lee, K.; Ambrose, Z.; Martin, T.D.; Oztop, I.; Mulky, A.; Julias, J.G.; Vandergraaff, N.; Baumann, J.G.; Wang, R.; Yuen, W. et al. Flexible use of nuclear import pathways by HIV-1. Cell Host Microbe 2010,7, 221-233) confirms that the viral capsid plays a key role in HIV-1 nuclear entry in both dividing and nondividing cells. The identification of mutations in the viral capsid that alter the virus’s dependence on host cell nucleoporins represents an important advance in this poorly understood stage of the virus life cycle.
Keywords: HIV-1; capsid; nuclear entry; TNPO3; nucleoporins HIV-1; capsid; nuclear entry; TNPO3; nucleoporins
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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Shah, V.B.; Aiken, C. HIV Nuclear Entry: Clearing the Fog. Viruses 2010, 2, 1190-1194.

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