Evidence map›Paper›PMID 19420080›Full record

ArticleJournal of virology2009

Variation in antagonism of the interferon response to rotavirus NSP1 results in differential infectivity in mouse embryonic fibroblasts.

N Feng, A Sen, H Nguyen, P Vo, Y Hoshino, E M Deal, H B Greenberg

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.5field-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

34 citing papers in PubMed, 56 citations in OpenAlex.

  1. Frontiers in microbiology · 2026
    Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Frontiers in immunology · 2021
    Article
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  12. Review
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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

7 authors at 3 institutions in 1 country.

N FengStanford University, Stanford, California, USA.
A Sen
H Nguyen
P Vo
Y Hoshino
E M Deal
H B Greenberg
Stanford University · USVA Palo Alto Health Care System · USNational Institute of Allergy and Infectious Diseases · US

Funding

Proteomics/GenomicsP30DK056339 · NIDDK · STANFORD UNIVERSITY · PI GREENBERG, HARRY BERNARD · 2001 to 2010
$10.4M
VIRAL GASTROENTERITIS--BASIS OF PROTECTION AND VIRULENCER01AI021362 · NIAID · STANFORD UNIVERSITY · PI GREENBERG, HARRY BERNARD · 1989 to 2014
$5.4M
Rotavirus Pathogenesis And Vaccine DevelopmentZ01AI000340 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI HOSHINO, YASUTAKA · 1985 to 2008
$388k
Genetic Studies Of Rotavirus Pathogenesis And Development Of Rotavirus VaccinesZIAAI000340 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI HOSHINO, YASUTAKA · 2009 to 2010
$342k
NIAID NIH HHS R01 AI021362NIAID NIH HHS R01 AI021362-24NIDDK NIH HHS P30 DK056339NIDDK NIH HHS P30DK56339
6 · The paper itself

Abstract

Rotavirus NSP1 has been shown to function as an E3 ubiquitin ligase that mediates proteasome-dependent degradation of interferon (IFN) regulatory factors (IRF), including IRF3, -5, and -7, and suppresses the cellular type I IFN response. However, the effect of rotavirus NSP1 on viral replication is not well defined. Prior studies used genetic analysis of selected reassortants to link NSP1 with host range restriction in the mouse, suggesting that homologous and heterologous rotaviruses might use their different abilities to antagonize the IFN response as the basis of their host tropisms. Using a mouse embryonic fibroblast (MEF) model, we demonstrate that heterologous bovine (UK and NCDV) and porcine (OSU) rotaviruses fail to effectively degrade cellular IRF3, resulting in IRF3 activation and beta IFN (IFN-beta) secretion. As a consequence of this failure, replication of these viruses is severely restricted in IFN-competent wild-type, but not in IFN-deficient (IFN-alpha/beta/gamma receptor- or STAT1-deficient) MEFs. On the other hand, homologous murine rotaviruses (ETD or EHP) or the heterologous simian rotavirus (rhesus rotavirus [RRV]) efficiently degrade cellular IRF3, diminish IRF3 activation and IFN-beta secretion and are not replication restricted in wild-type MEFs. Genetic reassortant analysis between UK and RRV maps the distinctive phenotypes of IFN antagonism and growth restriction in wild-type MEFs to NSP1. Therefore, there is a direct relationship between the replication efficiencies of different rotavirus strains in MEFs and strain-related variations in NSP1-mediated antagonism of the type I IFN response.

Indexed as

AnimalsCells, CulturedEmbryo, MammalianFibroblastsHumansInterferon-betaInterferon Regulatory Factor-3MiceMice, KnockoutRotavirusRotavirus InfectionsViral Nonstructural ProteinsVirus ReplicationInterferon-betaInterferon Regulatory Factor-3nsp1 protein, RotavirusViral Nonstructural Proteins

Identifiers

PMID19420080
PMCPMC2704795
OpenAlexW2165679960

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.