HIV infection triggers transcriptomic remodelling and a quiescence programme via KLF2 and the p53 pathway leading to proviral silencing.

In a landmark study published in Nature Microbiology, researchers have unveiled a revolutionary insight into the enigmatic interplay between HIV and the immune system's CD4+ T cells. The team led by Plasek Hegde and colleagues has elucidated a novel mechanism by which HIV commandeers the cellular machinery of these critical immune cells, reprogramming them into a state of profound quiescence and facilitating their entry into proviral latency.

HIV infection triggers transcriptomic remodelling and a quiescence programme via KLF2 and the p53 pathway leading to proviral silencing.

HIV infection triggers transcriptomic remodelling and a quiescence programme via KLF2 and the p53 pathway leading to proviral silencing.