Evidence map›Paper›PMID 31937650›Full record

ArticlemBio2020

The U-Rich Untranslated Region of the Hepatitis E Virus Induces Differential Type I and Type III Interferon Responses in a Host Cell-Dependent Manner.

Harini Sooryanarain, Connie L Heffron, Xiang-Jin Meng

Open access · goldAbstract read
In one paragraph

Article in mBio, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 21 citations in OpenAlex.

  1. Fatty acid regulation and phosphatidylethanolamine biosynthesis are important for hepatitis E virus replication.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Review
  3. Article
  4. Review
  5. Hepatitis E virus: from innate sensing to adaptive immune responses.Nature reviews. Gastroenterology & hepatology · 2024
    Review
  6. Review
  7. Article
  8. Review
  9. Immunobiology and Host Response to HEV.Advances in experimental medicine and biology · 2023
    Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Structural and molecular biology of hepatitis E virus.Computational and structural biotechnology journal · 2021
    Review
  17. 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

3 authors at 1 institution in 1 country.

Harini SooryanarainDepartment of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Blacksburg, Virginia, USA.
Connie L HeffronDepartment of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Blacksburg, Virginia, USA.
Xiang-Jin MengDepartment of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Blacksburg, Virginia, USA xjmeng@vt.edu.
Virginia Tech · US

Funding

A Chicken Model to Study Hepatitis E Virus PathogenesisR01AI050611 · NIAID · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI MENG, XIANG-JIN · 2002 to 2023
$6.1M
Mechanism of Hepatitis E Virus Replication and PathogenesisR01AI074667 · NIAID · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI MENG, XIANG-JIN · 2008 to 2016
$3.1M
NIAID NIH HHS R01 AI050611NIAID NIH HHS R01 AI074667
6 · The paper itself

Abstract

Hepatitis E virus (HEV), a single-strand positive-sense RNA virus, is an understudied but important human pathogen. The virus can establish infection at a number of host tissues, including the small intestine and liver, causing acute and chronic hepatitis E as well as certain neurological disorders. The retinoic acid-inducible gene I (RIG-I) pathway is essential to induce the interferon (IFN) response during HEV infection. However, the pathogen-associated motif patterns (PAMPs) in the HEV genome that are recognized by RIG-I remain unknown. In this study, we first identified that HEV RNA PAMPs derived from the 3' untranslated region (UTR) of the HEV genome induced higher levels of IFN mRNA, interferon regulatory factor-3 (IRF3) phosphorylation, and nuclear translocation than the 5' UTR of HEV. We revealed that the U-rich region in the 3' UTR of the HEV genome acts as a potent RIG-I PAMP, while the presence of poly(A) tail in the 3' UTR further increases the potency. We further demonstrated that HEV UTR PAMPs induce differential type I and type III IFN responses in a cell type-dependent fashion. Predominant type III IFN response was observed in the liver tissues of pigs experimentally infected with HEV as well as in HEV RNA PAMP-induced human hepatocytes

Indexed as

Immunity, Innate3' Untranslated Regions5' Untranslated RegionsAnimalsEnterocytesGenome, ViralHepatitis E virusHepatocytesHost Microbial InteractionsHumansInterferon LambdaInterferon Regulatory Factor-3InterferonsInterferon Type IPathogen-Associated Molecular Pattern MoleculesPhosphorylation3' Untranslated Regions5' Untranslated RegionsInterferon LambdaInterferon Regulatory Factor-3InterferonsInterferon Type IIRF3 protein, humanPathogen-Associated Molecular Pattern MoleculesUntranslated Regionshepatitis E virus (HEV)retinoic acid-inducible gene I (RIG-I)type-III IFNtype I interferon (IFN)U-rich region RNA PAMPs

Identifiers

PMID31937650
PMCPMC6960293
OpenAlexW2998957342

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.