Evidence map›Paper›PMID 20457596›Full record

ReviewThe Journal of biological chemistry2010

Induction and evasion of innate antiviral responses by hepatitis C virus.

Stanley M Lemon

Open access · hybridAbstract readReview
In one paragraph

Review in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 2% 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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Influenza Antiviral Subversion: Now the Host Is in on the Act.American journal of respiratory cell and molecular biology · 2021
    Article
  5. Article
  6. Innate Immunity to Enteric Hepatitis Viruses.Cold Spring Harbor perspectives in medicine · 2019
    Review
  7. Review
  8. Systematic identification of anti-interferon function on hepatitis C virus genome reveals p7 as an immune evasion protein.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  9. Article
  10. Article
  11. Toll-like receptor 3-activated macrophages confer anti-HCV activity to hepatocytes through exosomes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Genetic variants at the IFNL3 locus and their association with hepatitis C virus infections reveal novel insights into host-virus interactions.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2014
    Review
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

1 author at 1 institution in 1 country.

Stanley M LemonDivision of Infectious Disease, Department of Medicine, Center for Translational Immunology, Inflammatory Diseases Institute, Lineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7030, USA.
University of North Carolina at Chapel Hill · US

Funding

Virus-Host Interactions in Hepatitis C Virus (HCV) InfectionsU19AI040035 · NIAID · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI GALE, MICHAEL · 1996 to 2009
$12.0M
Intrahepatic IRF-3 and NF-kB Signaling and Interferon Responses in Hepatitis CR21AI081058 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI LEMON, STANLEY M. · 2009 to 2010
$413k
NIAID NIH HHS R21 AI081058NIAID NIH HHS R21-AI081058-1NIAID NIH HHS U19 AI040035NIAID NIH HHS U19-AI40035-14
6 · The paper itself

Abstract

Persistent hepatitis C virus infection is associated with progressive hepatic fibrosis and liver cancer. Acute infection evokes several distinct innate immune responses, but these are partially or completely countered by the virus. Hepatitis C virus proteins serve dual functions in replication and immune evasion, acting to disrupt cellular signaling pathways leading to interferon synthesis, subvert Jak-STAT signaling to limit expression of interferon-stimulated genes, and block antiviral activities of interferon-stimulated genes. The net effect is a multilayered evasion of innate immunity, which negatively influences the subsequent development of antigen-specific adaptive immunity, thereby contributing to virus persistence and resistance to therapy.

Indexed as

Immune EvasionImmunity, InnateAnimalsHepacivirusHepatitis CHumansLiverSignal Transduction

Identifiers

PMID20457596
PMCPMC2906263
OpenAlexW2018167033

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.