HIV-1 weaponizes T-cell signals to open nuclear pores and infect resting cells
TL;DR
resting CD4+ T cells are normally resistant to cell-free HIV-1 due to a bottleneck at capsid nuclear import at the nuclear pore, but during cell–cell spread, HIV-1 triggers CD4–LCK signaling that activates CDK1, remodeling nucleoporins and the NPC to boost nuclear import and license infection; this cell–cell spread–driven mechanism explains why resting T cells can be infected in vivo and why cell-free virus is less effective.
- HIV-1 signalling remodels nuclear pores to licence infection Nature
- HIV-1 Remodels Nuclear Pores in Resting CD4+ T Cells to Facilitate Infection geneonline.com
- HIV-1 Alters Nuclear Pores to Enable Infection Bioengineer.org
- Queen Mary University of London: Scientists discover how HIV hijacks a cellular 'gateway' to infect resting immune cells European AIDS Treatment Group
- Scientists discover how HIV hijacks a cellular 'gateway' to infect resting immune cells Queen Mary University of London
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