2020
RUNX Binding Sites Are Enriched in Herpesvirus Genomes, and RUNX1 Overexpression Leads to Herpes Simplex Virus 1 Suppression
Kim DJ, Khoury-Hanold W, Jain PC, Klein J, Kong Y, Pope SD, Ge W, Medzhitov R, Iwasaki A. RUNX Binding Sites Are Enriched in Herpesvirus Genomes, and RUNX1 Overexpression Leads to Herpes Simplex Virus 1 Suppression. Journal Of Virology 2020, 94: 10.1128/jvi.00943-20. PMID: 32878886, PMCID: PMC7592204, DOI: 10.1128/jvi.00943-20.Peer-Reviewed Original ResearchConceptsDorsal root gangliaHSV-1 infectionNumerous viral genesHSV-2Sensory neuronsHost transcription factorsHSV-1 genomeHSV-1Dorsal root ganglion neuronsViral gene expressionMouse DRG neuronsLifelong latent infectionViral genesKnockdown of RUNX1Herpes simplex virus 1Simplex virus 1DRG neuronsGanglion neuronsRoot gangliaOverall infectionViral gene transcriptionLatent infectionHSV-2 genomeInfectionNeuroblastoma cells
2019
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