Evidence map›Paper›PMID 25766293›Full record

ArticleCell host & microbe2015

Poxvirus decapping enzymes enhance virulence by preventing the accumulation of dsRNA and the induction of innate antiviral responses.

Shin-Wu Liu, George C Katsafanas, Ruikang Liu, Linda S Wyatt, Bernard Moss

Open access · bronzeAbstract read
In one paragraph

Article in Cell host & microbe, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

74 citing papers in PubMed, 105 citations in OpenAlex.

  1. Perturbation of RNA homeostasis impairs mitochondrial respiration during poxvirus infection through excess RNA accumulation.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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  12. RNA recognition by PKR during DNA virus infection.Journal of medical virology · 2024
    Review
  13. Article
  14. Article
  15. Article
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  17. Review
  18. Review
  19. Monkeypox virus: The changing facets of a zoonotic pathogen.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2022
    Review
  20. Ribosomes in poxvirus infection.Current opinion in virology · 2022
    Review

14 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Shin-Wu LiuLaboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892-3210, USA.
George C KatsafanasLaboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892-3210, USA.
Ruikang LiuLaboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892-3210, USA.
Linda S WyattLaboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892-3210, USA.
Bernard MossLaboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892-3210, USA. Electronic address: bmoss@nih.gov.
National Institute of Allergy and Infectious Diseases · US

Funding

Poxvirus Gene Expression and DNA ReplicationZIAAI000307 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MOSS, BERNARD · 2009 to 2025
$14.6M
Poxvirus pathogenesis and immunityZIAAI000979 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MOSS, BERNARD · 2009 to 2022
$12.7M
Intramural NIH HHS ZIA AI000979
6 · The paper itself

Abstract

Poxvirus replication involves synthesis of double-stranded RNA (dsRNA), which can trigger antiviral responses by inducing phosphorylation-mediated activation of protein kinase R (PKR) and stimulating 2'5'-oligoadenylate synthetase (OAS). PKR inactivates the translation initiation factor eIF2α via phosphorylation, while OAS induces the endonuclease RNase L to degrade RNA. We show that poxvirus decapping enzymes D9 and D10, which remove caps from mRNAs, inhibit these antiviral responses by preventing dsRNA accumulation. Catalytic site mutations of D9 and D10, but not of either enzyme alone, halt vaccinia virus late protein synthesis and inhibit virus replication. Infection with the D9-D10 mutant was accompanied by massive mRNA reduction, cleavage of ribosomal RNA, and phosphorylation of PKR and eIF2α that correlated with a ∼ 15-fold increase in dsRNA compared to wild-type virus. Additionally, mouse studies show extreme attenuation of the mutant virus. Thus, vaccinia virus decapping, in addition to targeting mRNAs for degradation, prevents dsRNA accumulation and anti-viral responses.

Indexed as

Immunity, InnateVirus Replication2',5'-Oligoadenylate SynthetaseAnimalsCell LineeIF-2 KinaseEndoribonucleasesEukaryotic Initiation Factor-2HumansRNA, Double-StrandedVaccinia virusViral ProteinsVirulence2',5'-Oligoadenylate SynthetaseeIF-2 KinaseEndoribonucleasesEukaryotic Initiation Factor-2mRNA decapping enzymesRNA, Double-StrandedViral Proteins

Identifiers

PMID25766293
PMCPMC4359750
OpenAlexW2160804763

What OpenQuestion holds

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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.