Evidence map›Paper›PMID 17459917›Full record

ArticleJournal of virology2007

Inhibition of the alpha/beta interferon response by mouse hepatitis virus at multiple levels.

Jessica K Roth-Cross, Luis Martínez-Sobrido, Erin P Scott, Adolfo García-Sastre, Susan R Weiss

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
12.4field-weighted citation impact, top 1% 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

71 citing papers in PubMed, 88 citations in OpenAlex.

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  10. Potential role of interferons in treating COVID-19 patients.International immunopharmacology · 2021
    Review
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11 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Jessica K Roth-CrossDepartment of Microbiology, University of Pennsylvania, School of Medicine, 36th Street and Hamilton Walk, Philadelphia, PA 19104-6076, USA.
Luis Martínez-Sobrido
Erin P Scott
Adolfo García-Sastre
Susan R Weiss
University of Pennsylvania · USIcahn School of Medicine at Mount Sinai · US

Funding

Technological Development ComponentU19AI062623 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI MORAN, THOMAS M · 2004 to 2009
$21.3M
Mechanisms for viral evasion of innate immune responseP01AI052106 · NIAID · UNIVERSITY OF WASHINGTON · PI PALESE, PETER · 2002 to 2006
$3.4M
TRAINING IN NEUROVIROLOGY AND NEUROIMMUNOLOGYT32NS007180 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI WEISS, SUSAN R · 1985 to 2018
$2.8M
Molecular Biology of Coronavirus Induced DemyelinationR01AI060021 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI WEISS, SUSAN R · 2003 to 2013
$2.7M
Neurovirulence of murine coronavirus: roles of viral genesR01NS054695 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI WEISS, SUSAN R · 2006 to 2010
$1.7M
NIAID NIH HHS AI-52106NIAID NIH HHS AI-60021NIAID NIH HHS N01 AI060021NIAID NIH HHS P01 AI052106NIAID NIH HHS U19 AI062623NIAID NIH HHS U19 AI-62623NINDS NIH HHS NS-54695NINDS NIH HHS R01 NS054695NINDS NIH HHS T32 NS007180
6 · The paper itself

Abstract

Mouse hepatitis virus (MHV) was used as a model to study the interaction of coronaviruses with the alpha/beta interferon (IFN-alpha/beta) response. While MHV strain A59 appeared to induce IFN-beta gene transcription and low levels of nuclear translocation of the IFN-beta transcription factor interferon regulatory factor 3 (IRF-3), MHV did not induce IFN-beta protein production during the course of infection in L2 mouse fibroblast cells. In addition, MHV was able to significantly decrease the level of IFN-beta protein induced by both Newcastle disease virus (NDV) and Sendai virus infections, without targeting it for proteasomal degradation and without altering the nuclear translocation of IRF-3 or IFN-beta mRNA production or stability. These results indicate that MHV infection causes an inhibition of IFN-beta production at a posttranscriptional level, without altering RNA or protein stability. In contrast, MHV induced IFN-beta mRNA and protein production in the brains of infected animals, suggesting that the inhibitory mechanisms observed in vitro are not enough to prevent IFN-alpha/beta production in vivo. Furthermore, MHV replication is highly resistant to IFN-alpha/beta action, as indicated by unimpaired MHV replication in L2 cells pretreated with IFN-beta. However, when L2 cells were coinfected with MHV and NDV in the presence of IFN-beta, NDV, but not MHV, replication was inhibited. Thus, rather than disarming the antiviral activity induced by IFN-beta pretreatment completely, MHV may be inherently resistant to some aspects of the antiviral state induced by IFN-beta. These findings show that MHV employs unique strategies to circumvent the IFN-alpha/beta response at multiple steps.

Indexed as

Active Transport, Cell NucleusAnimalsAntiviral AgentsCell NucleusChlorocebus aethiopsFibroblastsHepatitis, Viral, AnimalInterferon-alphaInterferon-betaInterferon Regulatory Factor-3MaleMiceMurine hepatitis virusNewcastle disease virusProteasome Endopeptidase ComplexRNA, MessengerAntiviral AgentsInterferon-alphaInterferon-betaInterferon Regulatory Factor-3Irf3 protein, mouseProteasome Endopeptidase ComplexRNA, Messenger

Identifiers

PMID17459917
PMCPMC1933268
OpenAlexW2070904890

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.