Evidence map›Paper›PMID 31717991›Full record

ArticleViruses2019

The Capsid Protein of Hepatitis E Virus Inhibits Interferon Induction via Its N-terminal Arginine-Rich Motif.

Shaoli Lin, Yonglin Yang, Yuchen Nan, Zexu Ma, Liping Yang, Yan-Jin Zhang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Viruses, 2019. 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
1.7field-weighted citation impact, top 16% 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, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Hepatitis E virus: from innate sensing to adaptive immune responses.Nature reviews. Gastroenterology & hepatology · 2024
    Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Characteristics and Functions of HEV Proteins.Advances in experimental medicine and biology · 2023
    Article
  13. Structural aspects of hepatitis E virus.Archives of virology · 2022
    Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
  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

6 authors at 1 institution in 2 countries.

Shaoli LinMolecular Virology Laboratory, VA-MD College of Veterinary Medicine and Maryland Pathogen Research Institute, University of Maryland, College Park, MD 20740, USA.ORCID 0000-0003-0835-5554
Yonglin YangMolecular Virology Laboratory, VA-MD College of Veterinary Medicine and Maryland Pathogen Research Institute, University of Maryland, College Park, MD 20740, USA.
Yuchen NanMolecular Virology Laboratory, VA-MD College of Veterinary Medicine and Maryland Pathogen Research Institute, University of Maryland, College Park, MD 20740, USA.ORCID 0000-0002-4442-8004
Zexu MaMolecular Virology Laboratory, VA-MD College of Veterinary Medicine and Maryland Pathogen Research Institute, University of Maryland, College Park, MD 20740, USA.
Liping YangMolecular Virology Laboratory, VA-MD College of Veterinary Medicine and Maryland Pathogen Research Institute, University of Maryland, College Park, MD 20740, USA.ORCID 0000-0001-9527-6015
Yan-Jin ZhangMolecular Virology Laboratory, VA-MD College of Veterinary Medicine and Maryland Pathogen Research Institute, University of Maryland, College Park, MD 20740, USA.ORCID 0000-0002-5847-3260
Virginia–Maryland College of Veterinary Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis E virus (HEV) causes predominantly acute and self-limiting hepatitis. However, in HEV-infected pregnant women, the case fatality rate because of fulminant hepatitis can be up to 30%. HEV infection is zoonotic for some genotypes. The HEV genome contains three open reading frames: ORF1 encodes the non-structural polyprotein involved in viral RNA replication; ORF2 encodes the capsid protein; ORF3 encodes a small multifunctional protein. Interferons (IFNs) play a significant role in the early stage of the host antiviral response. In this study, we discovered that the capsid protein antagonizes IFN induction. Mechanistically, the capsid protein blocked the phosphorylation of IFN regulatory factor 3 (IRF3) via interaction with the multiprotein complex consisting of mitochondrial antiviral-signaling protein (MAVS), TANK-binding kinase 1 (TBK1), and IRF3. The N-terminal domain of the capsid protein was found to be responsible for the inhibition of IRF3 activation. Further study showed that the arginine-rich-motif in the N-terminal domain is indispensable for the inhibition as mutations of any of the arginine residues abolished the blockage of IRF3 phosphorylation. These results provide further insight into HEV interference with the host innate immunity.

Indexed as

Host-Pathogen InteractionsProtein Interaction Domains and MotifsCapsid ProteinsGenotypeHepatitis EHepatitis E virusHumansInterferon Regulatory Factor-3InterferonsModels, BiologicalNerve Growth FactorsPhosphorylationPoly I-CProtein BindingProtein Serine-Threonine KinasesCapsid ProteinsInterferon Regulatory Factor-3InterferonsIRF3 protein, humanMANF protein, humanNerve Growth FactorsPoly I-CProtein Serine-Threonine KinasesTBK1 protein, humanarginine-rich motifhepatitis E virus (HEV), interferon (IFN), the capsid proteinIRF3 phosphorylation

Identifiers

PMID31717991
PMCPMC6928999
OpenAlexW2984096452

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.