Evidence map›Paper›PMID 37439556›Full record

ReviewmBio2023

Chromatin control of human cytomegalovirus infection.

Stephen M Matthews, Ian J Groves, Christine M O'Connor

Open access · goldAbstract readReview
In one paragraph

Review in mBio, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.9field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 18 citations in OpenAlex.

  1. Mechanisms and Determinants of CMV Reactivation in Kidney Transplantation.International journal of molecular sciences · 2026
    Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. N6-methyladenosine modification of HCMV IE1 transcript promotes the repressive state of viral genome to achieve latent infection.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  9. Review
  10. The ageing virus hypothesis: Epigenetic ageing beyond the Tree of Life.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Host-encoded CTCF regulates human cytomegalovirus latency via chromatin looping.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  17. Article
  18. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Stephen M MatthewsInfection Biology, Global Center for Pathogen and Human Health Research, Lerner Research Institute, Cleveland Clinic , Cleveland, Ohio, USA.ORCID 0000-0002-8968-225X
Ian J GrovesInfection Biology, Global Center for Pathogen and Human Health Research, Lerner Research Institute, Cleveland Clinic , Cleveland, Ohio, USA.ORCID 0000-0001-8882-6701
Christine M O'ConnorInfection Biology, Global Center for Pathogen and Human Health Research, Lerner Research Institute, Cleveland Clinic , Cleveland, Ohio, USA.ORCID 0000-0003-4943-3774
Cleveland Clinic Lerner College of Medicine · US

Funding

Manipulation of host factors that promote HCMV latencyR01AI150931 · NIAID · CLEVELAND CLINIC LERNER COM-CWRU · PI O'CONNOR, CHRISTINE M · 2021 to 2025
$2.4M
HCMV GPCR functions during latency and reactivationR01AI153348 · NIAID · CLEVELAND CLINIC LERNER COM-CWRU · PI O'CONNOR, CHRISTINE M · 2021 to 2025
$2.2M
NIAID NIH HHS R01 AI150931NIAID NIH HHS R01 AI153348
6 · The paper itself

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.

Indexed as

ChromatinCytomegalovirus InfectionsCytomegalovirusEpigenesis, GeneticGene Expression Regulation, ViralHistonesHumansVirus LatencyChromatinHistoneschromatinCMVcytomegalovirusepigeneticsherpesvirusHHVhistonetranscription factors

Identifiers

PMID37439556
PMCPMC10470543
OpenAlexW4384120429

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.