Kick and kill

HIV has a clever survival trick: it can hide in certain cells, lying dormant in a state called "latency." While modern antiretroviral therapy keeps the active virus under control, it cannot eliminate these hidden reservoirs, which means that HIV latency remains a major obstacle to a cure. In our recent study, we explored how glucocorticoid receptors (GRs) —proteins that respond to hormones such as cortisol—might influence HIV latency.

We discovered that AZD9567, a GR-modulating drug originally tested for rheumatoid arthritis, can reactivate latent HIV in multiple cell types. This reactivation happens through its effects on specific parts of the HIV genome, known as long terminal repeats (LTRs), which act like on-off-switches for the virus. Importantly, our findings suggest that AZD9567 could be a valuable addition to "kick-and-kill" strategies, where latent HIV is reactivated and then eliminated by the immune system or other treatments. The findings have been published in the Journal of Virology and can be found here.

Image: A snapshop of Dr. Fayyaz and Prof. Sauter, authors of the study, celebrating their collaborative effort to uncover new insights into HIV latency.