Evidence map›Paper›PMID 21683701›Full record

ArticleGastroenterology2011

Differential, type I interferon-mediated autophagic trafficking of hepatitis C virus proteins in mouse liver.

Mayura M Desai, Bin Gong, Tehsheng Chan, Robert A Davey, Lynn Soong, Andrey A Kolokoltsov, Jiaren Sun

Open access · bronzeAbstract read
In one paragraph

Article in Gastroenterology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Diverse Functions of Autophagy in Liver Physiology and Liver Diseases.International journal of molecular sciences · 2019
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Hepatitis C virus and autophagy.Biological chemistry · 2015
    Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Living in the liver: hepatic infections.Nature reviews. Immunology · 2012
    Review
  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

7 authors at 1 institution in 1 country.

Mayura M DesaiDepartment of Microbiology and Immunology, University of Texas Medical Branch at Galveston, Galveston, Texas 77555-1019, USA. madesai@utmb.edu
Bin Gong
Tehsheng Chan
Robert A Davey
Lynn Soong
Andrey A Kolokoltsov
Jiaren Sun
The University of Texas Medical Branch at Galveston · US

Funding

PATHOGENIC MECHANISMS OF CUTANEOUS LEISHMANIASISR01AI043003 · NIAID · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI SOONG, LYNN · 1999 to 2010
$2.3M
Immune Mechanisms of HCV Persistence and PathogenesisR01AI069142 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI SUN, JIAREN · 2007 to 2012
$2.0M
Pathogenic Mechanisms of Cutaneous LeishmaniasisR56AI043003 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI SOONG, LYNN · 2012 to 2012
$306k
NIAID NIH HHS AI043003NIAID NIH HHS AI069142NIAID NIH HHS R01 AI043003NIAID NIH HHS R01 AI069142NIAID NIH HHS R56 AI043003
6 · The paper itself

Abstract

BACKGROUND &

aimsThe hepatitis C virus (HCV) serine protease NS3/4A can cleave mitochondria-associated antiviral signaling protein (MAVS) and block retinoic acid-inducible gene I-mediated interferon (IFN) responses. Although this mechanism is thought to have an important role in HCV-mediated innate immunosuppression, its significance in viral persistence is not clear.

methodsWe generated transgenic mice that express the HCV NS3/4A proteins specifically in the liver and challenged the animals with a recombinant vesicular stomatitis virus, a synthetic HCV genome, IFN alfa, or IFN beta. We evaluated the effects of HCV serine protease on the innate immune responses and their interactions.

resultsExpression of HCV NS3/4A resulted in cleavage of intrahepatic MAVS; challenge of transgenic mice with vesicular stomatitis virus or a synthetic HCV genome induced strong, type I IFN-mediated responses that were not significantly lower than those of control mice. Different challenge agents induced production of different ratios of IFN alfa and beta, resulting in different autophagic responses and vesicular trafficking patterns of endoplasmic reticulum- and mitochondria-associated viral proteins. IFN beta promoted degradation of the viral proteins by the autolysosome. Variant isoforms of MAVS were associated with distinct, type I IFN-mediated autophagic responses; these responses have a role in trafficking of viral components to endosomal compartments that contain Toll-like receptor-3.

conclusionsIFN beta mediates a distinct autophagic mechanism of antiviral host defense. MAVS has an important role in type I IFN-induced autophagic trafficking of viral proteins.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsAutophagyBiological TransportDEAD Box Protein 58DEAD-box RNA HelicasesEndoplasmic ReticulumGene ExpressionHepacivirusImmunity, InnateInterferon-alphaInterferon-betaInterferon Regulatory Factor-1Interferon Type ILiverMiceAdaptor Proteins, Signal TransducingDdx58 protein, mouseDEAD Box Protein 58DEAD-box RNA HelicasesInterferon-alphaInterferon-betaInterferon Regulatory Factor-1Interferon Type IMap1lc3b protein, mouseMAVS protein, mouseMicrotubule-Associated ProteinsNS3 protein, hepatitis C virusNucleoside-TriphosphataseRecombinant ProteinsRNA, ViralSerine EndopeptidasesViral Nonstructural ProteinsViral Proteases

Identifiers

PMID21683701
PMCPMC3152629
OpenAlexW2068320176

What OpenQuestion holds

Textmetadata
LicenceTDM
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.