Evidence map›Paper›PMID 22868377›Full record

ReviewSeminars in immunopathology2013

Innate immune responses in hepatitis C virus infection.

Kui Li, Stanley M Lemon

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in immunopathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. The regulation of innate antiviral immunity by TRIM56.Infectious diseases & immunity · 2025
    Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. HCV and tumor-initiating stem-like cells.Frontiers in physiology · 2022
    Review
  10. IntrahepaticViruses · 2021
    Article
  11. Review
  12. The Role of the RNA-RNA Interactome in the Hepatitis C Virus Life Cycle.International journal of molecular sciences · 2020
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

2 authors at 2 institutions in 1 country.

Kui LiDepartment of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, USA.
Stanley M Lemon
University of North Carolina at Chapel Hill · USUniversity of Tennessee Health Science Center · 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
Micro-RNA 122 and Chronic Hepatitis CR01AI095690 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI LEMON, STANLEY M. · 2011 to 2020
$3.7M
Role of TLR3 Signaling in Control of HCVR01AI069285 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI LI, KUI · 2007 to 2016
$2.5M
Impact of HCV NS3/4A Protease on Host Innate ImmunityR21DA018054 · NIDA · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI LI, KUI · 2003 to 2004
$302k
Role of TLR3 Signaling in Control of HCVR56AI069285 · NIAID · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI LI, KUI · 2012 to 2012
$300k
NIAID NIH HHS AI-040035NIAID NIH HHS AI-069285NIAID NIH HHS AI-095690NIAID NIH HHS R01 AI069285NIAID NIH HHS R01 AI095690NIAID NIH HHS R56 AI069285NIAID NIH HHS U19 AI040035NIDA NIH HHS DA-018054NIDA NIH HHS R21 DA018054
6 · The paper itself

Abstract

Hepatitis C virus (HCV) is a major causative agent of chronic hepatitis and hepatocellular carcinoma worldwide and thus poses a significant public health threat. A hallmark of HCV infection is the extraordinary ability of the virus to persist in a majority of infected people. Innate immune responses represent the front line of defense of the human body against HCV immediately after infection. They also play a crucial role in orchestrating subsequent HCV-specific adaptive immunity that is pivotal for viral clearance. Accumulating evidence suggests that the host has evolved multifaceted innate immune mechanisms to sense HCV infection and elicit defense responses, while HCV has developed elaborate strategies to circumvent many of these. Defining the interplay of HCV with host innate immunity reveals mechanistic insights into hepatitis C pathogenesis and informs approaches to therapy. In this review, we summarize recent advances in understanding innate immune responses to HCV infection, focusing on induction and effector mechanisms of the interferon antiviral response as well as the evasion strategies of HCV.

Indexed as

HepacivirusHepatitis CHumansImmune EvasionImmunity, InnateInterferonsReceptors, Retinoic AcidToll-Like Receptor 3InterferonsPLAAT4 protein, humanReceptors, Retinoic AcidTLR3 protein, humanToll-Like Receptor 3

Identifiers

PMID22868377
PMCPMC3732459
OpenAlexW2011552383

What OpenQuestion holds

Textmetadata
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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.