Metabolic reprogramming of CD4⁺ T cells by Zaprinast induces HIV-1 latency reversal ex vivo.

Date publication

juin 2026

Journal

Retrovirology

Auteurs

Membres identifiés du Cancéropôle Est :
Pr ROHR Olivier

Tous les auteurs :
De Masson d'Autume V, LeDouce V, Dutilleul A, O'Reilly S, François N, Formiconi E, Angieladis M, Pilosio L, Bendoumou M, Leon AG, Alalwan D, Moore E, McGinty T, Valle-Casuso JC, Macken A, Rohr O, Van Lint C, Sáez-Cirión A, Cotter A, Feeney E, Mallon PWG, Gautier WV

Lien Pubmed

https://www.ncbi.nlm.nih.gov/pubmed/42288905

Résumé

HIV-1 latency and persistence of viral reservoirs within memory CD4 T cells remain a fundamental obstacle to achieving a cure despite suppressive antiviral treatments. HIV-1 persistence is sustained by the dynamic interactions between viral regulatory mechanisms and the host cellular environment. At the intersection between immunometabolism and virology, the quiescent metabolic profile of resting CD4 T cells, defined as the balance between oxidative phosphorylation (OXPHOS) and aerobic glycolysis, supports the long-term maintenance of latent viral reservoirs. Existing "Shock and Kill" strategies have shown limited clinical impact, partly due to the metabolic constraints that limit robust viral reactivation. Targeting metabolic junctions to overcome this barrier may provide a complementary therapeutic avenue.

Référence

Retrovirology. 2026 06 13;: