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Glycolytic metabolism has been identified as a determinant of susceptibility to HIV\u20101 infection, but its role in the development and maintenance of HIV\u20101 latency has not been elucidated. By combining transcriptomic, proteomic, and metabolomic analyses, we here show that transition to latent HIV\u20101 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\n                    <jats:sup>+<\/jats:sup>\n                    \/NADH. Consequently, infected cells rely on the parallel pentose phosphate pathway and its main product, NADPH, fueling antioxidant pathways maintaining HIV\u20101 latency. Of note, blocking NADPH downstream effectors, thioredoxin and glutathione, favors HIV\u20101 reactivation from latency in lymphoid and myeloid cellular models. This provides a \u201cshock and kill effect\u201d decreasing proviral DNA in cells from people living with HIV\/AIDS. Overall, our data show that downmodulation of glycolysis is a metabolic signature of HIV\u20101 latency that can be exploited to target latently infected cells with eradication strategies.\n                  <\/jats:p>","DOI":"10.15252\/emmm.202013901","type":"journal-article","created":{"date-parts":[[2021,7,20]],"date-time":"2021-07-20T09:56:54Z","timestamp":1626775014000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":65,"title":["Glycolysis downregulation is a hallmark of HIV\u20101 latency and sensitizes infected cells to oxidative stress"],"prefix":"10.1038","volume":"13","author":[{"given":"Iart Luca","family":"Shytaj","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Francesco 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