Epigenotypes of latent herpesvirus genomes.

摘要: Epigenotypes are modified cellular or viral genotypes which differ in transcriptional activity spite of having an identical (or nearly identical) DNA sequence. Restricted expression latent, episomal herpesvirus genomes is also due to epigenetic modifications. There no virus production (lytic replication, associated with the all genes) tight latency. In vitro experiments demonstrated that methylation could influence latent (and/or crucial lytic) promoters prototype strains belonging three subfamilies (α-, β-, and γ-herpesviruses). vivo, however, not a major regulator herpes simplex type 1 (HSV-1, human α-herpesvirus) gene neurons infected mice. these cells, promoter/enhancer region latency-associated transcripts (LATs) enriched acetyl histone H3, suggesting modifications may control HSV-1 latency terminally differentiated, quiescent neurons. Epstein-Barr (EBV, γ-herpesvirus) series neoplasms. Latent, EBV subject host cell-dependent (DNA methylation, binding proteins protein complexes, modifications). The distinct epigenotypes types, i.e., cell type-specific usage controlling growth transformation-associated genes. contribution mechanisms regulation variable. contributes silencing Wp Cp (alternative for coding nuclear antigens EBNA 1–6) LMP1p, LMP2Ap, LMP2Bp (promoters encoding transmembrane proteins). does control, Qp (a promoter EBNA1 only) lymphoblastoid lines (LCLs), although methylated Qp-reporter constructs silenced. invariably unmethylated probably switched off by repressor LCLs.