Glycolysis downregulation is a hallmark of HIV-1 latency and sensitizes infected cells to oxidative stress.

ABSTRACT: HIV-1 infects lymphoid and myeloid cells, which can harbor a latent proviral reservoir responsible for maintaining lifelong infection. Glycolytic metabolism has been identified as a determinant of susceptibility to HIV-1 infection, but its role in the development and maintenance of HIV-1 latency has not been elucidated. By combining transcriptomic, proteomic, and metabolomic analyses, we here show that transition to latent HIV-1 infection downregulates glycolysis, while viral reactivation by conventional stimuli reverts this effect. Decreased glycolytic output in latently infected cells is associated with downregulation of NAD⁺ /NADH. Consequently, infected cells rely on the parallel pentose phosphate pathway and its main product, NADPH, fueling antioxidant pathways maintaining

SUBMITTER: Shytaj IL 

PROVIDER: S-EPMC8350904 | biostudies-literature | 2021 Aug

REPOSITORIES: biostudies-literature