Apobec3A maintains HIV-1 latency through recruitment of epigenetic silencing machinery to the long terminal repeat
Taura M, Song E, Ho YC, Iwasaki A. Apobec3A maintains HIV-1 latency through recruitment of epigenetic silencing machinery to the long terminal repeat. Proceedings Of The National Academy Of Sciences Of The United States Of America 2019, 116: 2282-2289. PMID: 30670656, PMCID: PMC6369738, DOI: 10.1073/pnas.1819386116.Peer-Reviewed Original ResearchMeSH KeywordsCD4-Positive T-LymphocytesCell LineCytidine DeaminaseEpigenesis, GeneticGene Expression Regulation, ViralGene SilencingHIV InfectionsHIV Long Terminal RepeatHIV-1HumansNF-kappa BProtein BindingProtein Interaction Domains and MotifsProteinsSequence DeletionSp1 Transcription FactorVirus ActivationVirus LatencyConceptsHIV-1 latencyHIV-1 reactivationCD4 T cellsT cellsHuman primary CD4 T cellsInfected CD4 T cellsHIV-1-infected cellsPrimary CD4 T cellsLong terminal repeat regionHIV-1Therapeutic strategiesLower reactivationProviral DNALatency maintenanceTarget cellsLatency stateCell linesLong terminal repeatTerminal repeat regionMolecular mechanismsReactivationCellsKnockdownA3AUnexpected role