Abstract
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.
Highlights
Et al Flexible use of nuclear import pathways by HIV-1
By screening a library of mouse cDNAs for clones that would render cells resistant to HIV-1, the authors identified a form of the RNA cleavage polyadenylation and specificity factor CPSF6
The resulting truncated protein, CPSF6-358, is not an endogenously expressed splice variant of CPSF6, but resulted from random cDNA priming of the library
Summary
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. By screening a library of mouse cDNAs for clones that would render cells resistant to HIV-1, the authors identified a form of the RNA cleavage polyadenylation and specificity factor CPSF6. CPSF6-358 inhibited HIV-1 at an early postentry step in infection, a block that the authors narrowed down to the nuclear import step.
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