Evidence map›Paper›PMID 23097436›Full record

ArticleJournal of virology2013

Efficient herpes simplex virus 1 replication requires cellular ATR pathway proteins.

Kareem N Mohni, Alexander R Dee, Samantha Smith, April J Schumacher, Sandra K Weller

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

35 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Early Nuclear Events after Herpesviral Infection.Journal of clinical medicine · 2019
    Review
  15. Coalescing replication compartments provide the opportunity for recombination between coinfecting herpesviruses.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

Kareem N MohniDepartment of Molecular, Microbial and Structural Biology and the Molecular Biology and Biochemistry Graduate Program, University of Connecticut Health Center, Farmington, Connecticut, USA.
Alexander R Dee
Samantha Smith
April J Schumacher
Sandra K Weller
UConn Health · US

Funding

GENETICS OF HSV DNA REPLICATIONR01AI021747 · NIAID · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI WELLER, SANDRA K, WRIGHT, DENNIS L. · 1985 to 2024
$9.9M
GENETICS OF HSV DNA REPLICATIONR37AI021747 · NIAID · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI WELLER, SANDRA K · 1998 to 2007
$3.3M
Role of viral and cellular recombination proteins in HSV DNA replicationR01AI069136 · NIAID · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI WELLER, SANDRA K · 2006 to 2016
$3.1M
NIAID NIH HHS AI069136NIAID NIH HHS AI21747NIAID NIH HHS R01 AI021747NIAID NIH HHS R01 AI069136NIAID NIH HHS R37 AI021747
6 · The paper itself

Abstract

Herpes simplex virus 1 (HSV-1) is a double-stranded DNA virus that replicates in the nucleus of the host cell and is known to interact with several components of the cellular DNA-damage-signaling machinery. We have previously reported that the DNA damage response kinase, ATR, is specifically inactivated in HSV-1-infected cells. On the other hand, we have also shown that ATR and its scaffolding protein, ATRIP, are recruited to viral replication compartments, where they play beneficial roles during HSV-1 replication. In order to better understand this apparent discrepancy, we tested the hypothesis that some of the components of the ATR pathway may exert an antiviral effect on infection. In fact, we learned that all 10 of the canonical ATR pathway proteins are stable in HSV-infected cells and are recruited to viral replication compartments; furthermore, short hairpin RNA (shRNA) knockdown shows that several, including ATRIP, RPA70, TopBP1, Claspin, and CINP, are required for efficient HSV-1 replication. We also determined that activation of the ATR kinase prior to infection did not affect virus yield but did result in reduced levels of recombination between coinfecting viruses. Together, these data suggest that ATR pathway proteins are not antiviral per se but that activation of ATR signaling may have negative consequences during viral replication, such as inhibiting recombination.

Indexed as

Host-Pathogen InteractionsSignal TransductionVirus ReplicationAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCell LineHerpesvirus 1, HumanHumansProtein Serine-Threonine KinasesAtaxia Telangiectasia Mutated ProteinsATR protein, humanCell Cycle ProteinsProtein Serine-Threonine Kinases

Identifiers

PMID23097436
PMCPMC3536419
OpenAlexW2026623208

What OpenQuestion holds

Textmetadata
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.