Chromatin control of human cytomegalovirus infection
ABSTRACT Human cytomegalovirus (HCMV) is a betaherpesvirus that establishes lifelong infection in its host and can cause severe comorbidities in individuals with suppressed or compromised immune systems. The lifecycle of HCMV consists of lytic and latent phases, largely dependent upon the cell type...
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Format: | Article |
Language: | English |
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American Society for Microbiology
2023-08-01
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Series: | mBio |
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Online Access: | https://journals.asm.org/doi/10.1128/mbio.00326-23 |
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author | Stephen M. Matthews Ian J. Groves Christine M. O'Connor |
author_facet | Stephen M. Matthews Ian J. Groves Christine M. O'Connor |
author_sort | Stephen M. Matthews |
collection | DOAJ |
description | ABSTRACT Human cytomegalovirus (HCMV) is a betaherpesvirus that establishes lifelong infection in its host and can cause severe comorbidities in individuals with suppressed or compromised immune systems. The lifecycle of HCMV consists of lytic and latent phases, largely dependent upon the cell type infected and whether transcription from the major immediate early locus can ensue. Control of this locus, which acts as a critical “switch” region from where the lytic gene expression cascade originates, as well as regulation of the additional ~235 kilobases of virus genome, occurs through chromatinization with cellular histone proteins after infection. Upon infection of a host cell, an initial intrinsic antiviral response represses gene expression from the incoming genome, which is relieved in permissive cells by viral and host factors in concert. Latency is established in a subset of hematopoietic cells, during which viral transcription is largely repressed while the genome is maintained. As these latently infected cells differentiate, the cellular milieu and epigenetic modifications change, giving rise to the initial stages of virus reactivation from latency. Thus, throughout the cycle of infection, chromatinization, chromatin modifiers, and the recruitment of specific transcription factors influence the expression of genes from the HCMV genome. In this review, we discuss epigenetic regulation of the HCMV genome during the different phases of infection, with an emphasis on recent reports that add to our current perspective. |
first_indexed | 2024-03-12T11:41:17Z |
format | Article |
id | doaj.art-1baa590fe0aa4c9890996d03c17d6e98 |
institution | Directory Open Access Journal |
issn | 2150-7511 |
language | English |
last_indexed | 2024-03-12T11:41:17Z |
publishDate | 2023-08-01 |
publisher | American Society for Microbiology |
record_format | Article |
series | mBio |
spelling | doaj.art-1baa590fe0aa4c9890996d03c17d6e982023-08-31T15:04:20ZengAmerican Society for MicrobiologymBio2150-75112023-08-0114410.1128/mbio.00326-23Chromatin control of human cytomegalovirus infectionStephen M. Matthews0Ian J. Groves1Christine M. O'Connor2Infection Biology, Global Center for Pathogen and Human Health Research, Lerner Research Institute, Cleveland Clinic , Cleveland, Ohio, USAInfection Biology, Global Center for Pathogen and Human Health Research, Lerner Research Institute, Cleveland Clinic , Cleveland, Ohio, USAInfection Biology, Global Center for Pathogen and Human Health Research, Lerner Research Institute, Cleveland Clinic , Cleveland, Ohio, USAABSTRACT Human cytomegalovirus (HCMV) is a betaherpesvirus that establishes lifelong infection in its host and can cause severe comorbidities in individuals with suppressed or compromised immune systems. The lifecycle of HCMV consists of lytic and latent phases, largely dependent upon the cell type infected and whether transcription from the major immediate early locus can ensue. Control of this locus, which acts as a critical “switch” region from where the lytic gene expression cascade originates, as well as regulation of the additional ~235 kilobases of virus genome, occurs through chromatinization with cellular histone proteins after infection. Upon infection of a host cell, an initial intrinsic antiviral response represses gene expression from the incoming genome, which is relieved in permissive cells by viral and host factors in concert. Latency is established in a subset of hematopoietic cells, during which viral transcription is largely repressed while the genome is maintained. As these latently infected cells differentiate, the cellular milieu and epigenetic modifications change, giving rise to the initial stages of virus reactivation from latency. Thus, throughout the cycle of infection, chromatinization, chromatin modifiers, and the recruitment of specific transcription factors influence the expression of genes from the HCMV genome. In this review, we discuss epigenetic regulation of the HCMV genome during the different phases of infection, with an emphasis on recent reports that add to our current perspective.https://journals.asm.org/doi/10.1128/mbio.00326-23herpesvirusHHVepigeneticschromatincytomegalovirusCMV |
spellingShingle | Stephen M. Matthews Ian J. Groves Christine M. O'Connor Chromatin control of human cytomegalovirus infection mBio herpesvirus HHV epigenetics chromatin cytomegalovirus CMV |
title | Chromatin control of human cytomegalovirus infection |
title_full | Chromatin control of human cytomegalovirus infection |
title_fullStr | Chromatin control of human cytomegalovirus infection |
title_full_unstemmed | Chromatin control of human cytomegalovirus infection |
title_short | Chromatin control of human cytomegalovirus infection |
title_sort | chromatin control of human cytomegalovirus infection |
topic | herpesvirus HHV epigenetics chromatin cytomegalovirus CMV |
url | https://journals.asm.org/doi/10.1128/mbio.00326-23 |
work_keys_str_mv | AT stephenmmatthews chromatincontrolofhumancytomegalovirusinfection AT ianjgroves chromatincontrolofhumancytomegalovirusinfection AT christinemoconnor chromatincontrolofhumancytomegalovirusinfection |