Evidence map›Paper›PMID 33563816›Full record

ArticlemBio2021

Herpes Simplex Virus 1 Manipulates Host Cell Antiviral and Proviral DNA Damage Responses.

Max E Mertens, David M Knipe

Open access · goldAbstract read
In one paragraph

Article in mBio, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Expulsion of nuclear DNA to the cytoplasm after viral entry: A mechanism for activation of the cGAS pathway.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Host-directed novel mechanistic insights of doxorubicin reveal its efficacy against drug-resistant HSV-1 underscoring risks with oncolytic virotherapy.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2026
    Article
  9. Article
  10. Article
  11. Oncolytic HSV and cancer drug interactions: Current clinical status and future directions.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Nuclear interferon-stimulated gene product maintains heterochromatin on the herpes simplex viral genome to limit lytic infection.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  18. Article
  19. Article
  20. Review
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

2 authors at 1 institution in 1 country.

Max E MertensDepartment of Microbiology, Blavatnik Institute, Harvard Medical School, Boston, Massachusetts, USA.
David M KnipeDepartment of Microbiology, Blavatnik Institute, Harvard Medical School, Boston, Massachusetts, USA david_knipe@hms.harvard.edu.ORCID 0000-0003-1554-6236
Harvard University · US

Funding

Nuclear Sensing of Herpesviral DNAR01AI106934 · NIAID · HARVARD MEDICAL SCHOOL · PI KNIPE, DAVID M. · 2014 to 2021
$3.8M
Nuclear Sensing of Herpesviral DNAR56AI106934 · NIAID · HARVARD MEDICAL SCHOOL · PI KNIPE, DAVID M. · 2024 to 2024
$587k
The Role of the Nuclear Envelope in Antiviral Signaling and HSV-1 RestrictionF31AI129207 · NIAID · HARVARD MEDICAL SCHOOL · PI MERTENS, MAX ELDON · 2017 to 2019
$102k
NIAID NIH HHS F31 AI129207NIAID NIH HHS R01 AI106934NIAID NIH HHS R56 AI106934
6 · The paper itself

Abstract

Cells activate their DNA damage response (DDR) in response to DNA virus infection, including adenoviruses, papillomaviruses, polyomaviruses, and herpesviruses. In this study, we found that the DDR kinase pathways activated in normal human fibroblasts by herpes simplex virus 1 (HSV-1) input genomic DNA, HSV-1 replicating DNA, and progeny DNA and in uninfected cells treated with etoposide are different. We also found using clustered regularly interspaced palindromic repeat (CRISPR)-Cas9 technology that different host gene products are required for the DDR in uninfected versus infected cells. Individual DDR components can be proviral or antiviral in that ataxia-telangiectasia mutated (ATM) and p53 promote and Mre11 restricts replication of ICP0-null HSV-1, but ICP0 expression eliminates these DDR effects. Thus, in total, these results argue that HSV-1 manipulates the host cell DDR to utilize specific components for its optimal replication while inactivating the antiviral aspects of the DDR.

Indexed as

DNA DamageHost-Pathogen InteractionsAntiviral AgentsAtaxia Telangiectasia Mutated ProteinsCell LineClustered Regularly Interspaced Short Palindromic RepeatsDNA, ViralFibroblastsForeskinGenome, ViralHerpesvirus 1, HumanHumansMaleProvirusesVirus ReplicationAntiviral AgentsAtaxia Telangiectasia Mutated ProteinsDNA, ViralDNA damage responseherpes simplex virusviral replication

Identifiers

PMID33563816
PMCPMC7885110
OpenAlexW3126996936

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.