Hydrogen sulfide blocks HIV rebound by maintaining mitochondrial bioenergetics and redox homeostasis.

ABSTRACT: A fundamental challenge in human immunodeficiency virus (HIV) eradication is to understand how the virus establishes latency, maintains stable cellular reservoirs, and promotes rebound upon interruption of antiretroviral therapy (ART). Here, we discovered an unexpected role of the ubiquitous gasotransmitter hydrogen sulfide (H₂S) in HIV latency and reactivation. We show that reactivation of HIV is associated with downregulation of the key H₂S producing enzyme cystathionine-γ-lyase (CTH) and reduction in endogenous H₂S. Genetic silencing of CTH disrupts redox homeostasis, impairs mitochondrial function, and remodels the transcriptome of latent cells to trigger HIV reactivation. Chemical complementation of CTH activity using a slow-releasing H₂S do

SUBMITTER: Pal VK 

PROVIDER: S-EPMC8660018 | biostudies-literature | 2021 Nov

REPOSITORIES: biostudies-literature