Evidence map›Paper›PMID 25724417›Full record

ReviewVirology2015

Silencing the alarms: Innate immune antagonism by rotavirus NSP1 and VP3.

Marco Morelli, Kristen M Ogden, John T Patton

Open access · greenAbstract readReview
In one paragraph

Review in Virology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Review
  3. Frontiers in microbiology · 2026
    Review
  4. Frontiers in cellular and infection microbiology · 2025
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Microorganisms · 2021
    Review
  14. Review
  15. Review
  16. Review
  17. Human norovirus exhibits strain-specific sensitivity to host interferon pathways in human intestinal enteroids.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  18. Understanding the penetrance of intrinsic protein disorder in rotavirus proteome.International journal of biological macromolecules · 2020
    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

3 authors at 1 institution in 1 country.

Marco MorelliRotavirus Molecular Biology Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Kristen M OgdenRotavirus Molecular Biology Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
John T PattonRotavirus Molecular Biology Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: jpattn76@vt.edu.
National Institutes of Health · US

Funding

Modification Of The Antigenicity & Virulence Of Rotaviruses By Reverse GeneticsZIAAI000788 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI PATTON, JOHN · 2009 to 2015
$4.2M
MECHANISM OF ROTAVIRUS GENOME REPLICATION AND PACKAGINGZ01AI000754 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI PATTON, JOHN · 1996 to 2008
$1.1M
MODIFICATION OF THE ANTIGENICITY &VIRULENCE OF ROTAVIRUSES BY REVERSE GENETICSZ01AI000788 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI PATTON, JOHN · 1997 to 2008
$1.1M
Intramural NIH HHS Z01 AI000754Intramural NIH HHS Z01 AI000788Intramural NIH HHS ZIA AI000788NIAID NIH HHS Z1A AI000754NIAID NIH HHS Z1A AI000788
6 · The paper itself

Abstract

The innate immune response involves a broad array of pathogen sensors that stimulate the production of interferons (IFNs) to induce an antiviral state. Rotavirus, a significant cause of childhood gastroenteritis and a member of the Reoviridae family of segmented, double-stranded RNA viruses, encodes at least two direct antagonists of host innate immunity: NSP1 and VP3. NSP1, a putative E3 ubiquitin ligase, mediates the degradation of cellular factors involved in both IFN induction and downstream signaling. VP3, the viral capping enzyme, utilizes a 2H-phosphodiesterase domain to prevent activation of the cellular oligoadenylate synthase (OAS)/RNase L pathway. Computational, molecular, and biochemical studies have provided key insights into the structural and mechanistic basis of innate immune antagonism by NSP1 and VP3 of group A rotaviruses (RVA). Future studies with non-RVA isolates will be essential to understand how other rotavirus species evade host innate immune responses.

Indexed as

Host-Pathogen InteractionsImmune EvasionImmunity, InnateCapsid ProteinsRotavirusViral Nonstructural ProteinsCapsid Proteinsnsp1 protein, RotavirusViral Nonstructural ProteinsVP3 protein, RotavirusInnate immunityInterferon signaling pathwayNF-κBOAS/RNase L pathwayRotavirusViral E3 ubiquitin ligaseViral phosphodiesteraseβ-TrCP

Identifiers

PMID25724417
PMCPMC4940189
OpenAlexW2095406871

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.