Cell-to-cell spread primes the nuclear pore for HIV-1.

Cell-to-cell spread reprograms resting CD4⁺ T cells to permit infection. Mesner et al. show that contact between infected and uninfected T cells triggers CD4-LCK signaling, activating CDK1 independently of cell-cycle entry to remodel the nuclear pore, enabling HIV-1 nuclear import and overcoming a major barrier in resting T cells.