De novo synthesis of VP16 coordinates the exit from HSV latency in vivo.
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A comparison of herpes simplex virus type 1 and varicella-zoster virus latency and reactivationThe molecular basis of herpes simplex virus latencyA cultured affair: HSV latency and reactivation in neuronsLocal CD4 and CD8 T-cell reactivity to HSV-1 antigens documents broad viral protein expression and immune competence in latently infected human trigeminal gangliaHerpes simplex virus and the lexicon of latency and reactivation: a call for defining terms and building an integrated collective frameworkTransient reversal of episome silencing precedes VP16-dependent transcription during reactivation of latent HSV-1 in neuronsRestarting Lytic Gene Transcription at the Onset of Herpes Simplex Virus ReactivationCellular heterogeneity and live cell arrays.Virologic and immunologic evidence of multifocal genital herpes simplex virus 2 infection.Neuronal Stress Pathway Mediating a Histone Methyl/Phospho Switch Is Required for Herpes Simplex Virus Reactivation.Pseudomonas aeruginosa biofilm infections in cystic fibrosis: insights into pathogenic processes and treatment strategies.Role of nuclear factor Y in stress-induced activation of the herpes simplex virus type 1 ICP0 promoterHerpes simplex virus VP16, but not ICP0, is required to reduce histone occupancy and enhance histone acetylation on viral genomes in U2OS osteosarcoma cells.Retrograde axon transport of herpes simplex virus and pseudorabies virus: a live-cell comparative analysis.The major determinant for addition of tegument protein pUL48 (VP16) to capsids in herpes simplex virus type 1 is the presence of the major tegument protein pUL36 (VP1/2)Directional transneuronal spread of α-herpesvirus infection.Herpes simplex type I (HSV-1) infection of the nervous system: is an immune response a good thing?Transcription of the herpes simplex virus 1 genome during productive and quiescent infection of neuronal and nonneuronal cells.Antagonistic determinants controlling replicative and latent states of human cytomegalovirus infectionIn vivo reactivation of latent herpes simplex virus 1 in mice can occur in the brain before occurring in the trigeminal ganglionEntry of herpes simplex virus type 1 (HSV-1) into the distal axons of trigeminal neurons favors the onset of nonproductive, silent infectionUpdate on herpes virus infections of the nervous system.Centromere architecture breakdown induced by the viral E3 ubiquitin ligase ICP0 protein of herpes simplex virus type 1.The CoREST/REST repressor is both necessary and inimical for expression of herpes simplex virus genes.Tegument protein control of latent herpesvirus establishment and animation.Varicella zoster virus latency.Characterization of neuronal populations in the human trigeminal ganglion and their association with latent herpes simplex virus-1 infection.A forward phenotypically driven unbiased genetic analysis of host genes that moderate herpes simplex virus virulence and stromal keratitis in mice.The checkpoints of viral gene expression in productive and latent infection: the role of the HDAC/CoREST/LSD1/REST repressor complexCharacterization of herpes simplex virus 2 primary microRNA Transcript regulationHSV-1 gene expression from reactivated ganglia is disordered and concurrent with suppression of latency-associated transcript and miRNAsCellular transcription factors induced in trigeminal ganglia during dexamethasone-induced reactivation from latency stimulate bovine herpesvirus 1 productive infection and certain viral promoters.The HSV-1 Latency-Associated Transcript Functions to Repress Latent Phase Lytic Gene Expression and Suppress Virus Reactivation from Latently Infected NeuronsControl of viral latency in neurons by axonal mTOR signaling and the 4E-BP translation repressor.Latency Entry of Herpes Simplex Virus 1 Is Determined by the Interaction of Its Genome with the Nuclear EnvironmentAttenuation of Histone Methyltransferase KRYPTONITE-mediated transcriptional gene silencing by Geminivirus.Epstein-Barr Virus (EBV) Tegument Protein BGLF2 Promotes EBV Reactivation through Activation of the p38 Mitogen-Activated Protein Kinase.An investigation of herpes simplex virus promoter activity compatible with latency establishment reveals VP16-independent activation of immediate-early promoters in sensory neuronesC-terminal trans-activation sub-region of VP16 is uniquely required for forskolin-induced herpes simplex virus type 1 reactivation from quiescently infected-PC12 cells but not for replication in neuronally differentiated-PC12 cells.DNA damage promotes herpes simplex virus-1 protein expression in a neuroblastoma cell line.
P2860
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P2860
De novo synthesis of VP16 coordinates the exit from HSV latency in vivo.
description
2009 nî lūn-bûn
@nan
2009 թուականի Մարտին հրատարակուած գիտական յօդուած
@hyw
2009 թվականի մարտին հրատարակված գիտական հոդված
@hy
2009年の論文
@ja
2009年論文
@yue
2009年論文
@zh-hant
2009年論文
@zh-hk
2009年論文
@zh-mo
2009年論文
@zh-tw
2009年论文
@wuu
name
De novo synthesis of VP16 coordinates the exit from HSV latency in vivo.
@ast
De novo synthesis of VP16 coordinates the exit from HSV latency in vivo.
@en
type
label
De novo synthesis of VP16 coordinates the exit from HSV latency in vivo.
@ast
De novo synthesis of VP16 coordinates the exit from HSV latency in vivo.
@en
prefLabel
De novo synthesis of VP16 coordinates the exit from HSV latency in vivo.
@ast
De novo synthesis of VP16 coordinates the exit from HSV latency in vivo.
@en
P2860
P1433
P1476
De novo synthesis of VP16 coordinates the exit from HSV latency in vivo.
@en
P2093
Chris M Preston
Nancy M Sawtell
P2860
P304
P356
10.1371/JOURNAL.PPAT.1000352
P577
2009-03-27T00:00:00Z