AI Article Synopsis
- HIV-1 and other lentiviruses can infect nondividing cells, but their method of crossing the nuclear membrane remains unclear.
- Recent research highlights the significant role of the viral capsid in HIV-1's entry into the nucleus, regardless of whether the cell is dividing.
- Discovering mutations in the viral capsid that affect the virus's reliance on host cell nucleoporins marks a key advancement in understanding this part of the virus life cycle.
Article 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 Microbe2010, 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.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3187605 | PMC |
| http://dx.doi.org/10.3390/v2051190 | DOI Listing |
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