Saba Valadkhan

This manuscript is accompanied by a News and Views in Nature Immunology. Many thanks to Drs. Melanie Ott and Zichong Li @TheOttLabfor authoring it. Here is the link: nature.com/articles/s4159

HIV infection reprogrammes CD4+ T cells for quiescence and entry into proviral latency - Nature Microbiology HIV infection triggers transcriptomic remodelling and a quiescence programme via KLF2 and the p53 pathway leading to proviral silencing.

This work was a collaboration between Valadkhan lab and Dr. Jonathan Karn's lab, with @LeahPlasek
and @persilon doing most of the experimental heavylifting, and funded by @NIDAnews and @NIAIDNews. Link to the manuscript: bit.ly/4nwyEQQ

So, formation of the latent HIV reservoir, the main barrier to #HIVcure, isn't a random process, but a deliberate survival strategy by HIV. This work has major implications for #EndHIV efforts by uncovering new therapeutic targets to address critical gaps in existing therapies.

We showed that post-integration expression of viral genes activates two key anti-proliferative pathways, p53 and KLF2, leading to strong MYC suppression, cellular quiescence, and notably, proviral latency in a subset of infected cells. We confirmed key results in cells from PWH.

We studied global gene expression patterns in CD4+ T cells at early time points after HIV infection. We also, for the first time, defined the mechanism of quiescence in CD4+ cells. The similarities were striking: HIV actively drives T cells into quiescence! How did this happen?

Excited to share our new manuscript in @NatureMicrobiol
uncovering a novel mechanism by which viruses orchestrate their survival in the host. We show that #HIV inherently induces the formation of a latent reservoir of viruses, guaranteeing its long-term survival in the host 🧵 #HIVresearch

HIV Reprograms CD4+ T Cells for Latency 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 Reprograms CD4+ T Cells for Latency

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…

HIV infection reprogrammes CD4+ T cells for quiescence and entry into proviral latency - Nature Microbiology HIV infection triggers transcriptomic remodelling and a quiescence programme via KLF2 and the p53 pathway leading to proviral silencing.

#HIV infection reprogrammes CD4+ T cells for quiescence and entry into proviral latency www.nature.com/articles/s41... (open access) @natmicrobiol.nature.com

Our lncRNA-in-brain review is out in @natrevneuro.nature.com

✨ The emerging roles of long noncoding RNAs in the brain

We discuss 🧬 lncRNA roles in brain development, synaptic function, learning, & behavior
💡 Therapeutic potential and future directions.
@unswrna.bsky.social @unswbabs.bsky.social

HIV infection reprogrammes CD4+ T cells for quiescence and entry into proviral latency - Nature Microbiology HIV infection triggers transcriptomic remodelling and a quiescence programme via KLF2 and the p53 pathway leading to proviral silencing.

#NewResearch

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

#MicroSky 🦠

www.nature.com/articles/s41...

HIV infection of CD4 T cells drives KLF2 and p53 signaling, which downregulate MYC and proliferation pathways, resulting in proviral transcriptional silencing to enhance latent reservoir formation @natmicrobiol.nature.com @saba-valadkhan.bsky.social
www.nature.com/articles/s41...