Evidence map›Paper›PMID 28727933›Full record

ArticleVirulence2018

Genotype-specific acquisition, evolution and adaptation of characteristic mutations in hepatitis E virus.

Aqsa Ikram, Mohamad S Hakim, Jian-Hua Zhou, Wenshi Wang, Maikel P Peppelenbosch, Qiuwei Pan

Open access · goldAbstract readComparative Study
In one paragraph

Article in Virulence, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Antiviral Candidates for Treating Hepatitis E Virus Infection.Antimicrobial agents and chemotherapy · 2019
    Article
  9. Article
  10. Reply to the query "Chronic hepatitis E virus infection by genotype 1".Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2018
    Article
  11. Chronic hepatitis E virus infection by genotype 1-Don't stop looking yet!Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2018
    Article
  12. Article
  13. Hepatitis E: an underestimated emerging threat.Therapeutic advances in infectious disease
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 3 countries.

Aqsa Ikrama Department of Gastroenterology and Hepatology , Erasmus MC-University Medical Center , Rotterdam , the Netherlands.
Mohamad S Hakima Department of Gastroenterology and Hepatology , Erasmus MC-University Medical Center , Rotterdam , the Netherlands.
Jian-Hua Zhoua Department of Gastroenterology and Hepatology , Erasmus MC-University Medical Center , Rotterdam , the Netherlands.
Wenshi Wanga Department of Gastroenterology and Hepatology , Erasmus MC-University Medical Center , Rotterdam , the Netherlands.
Maikel P Peppelenboscha Department of Gastroenterology and Hepatology , Erasmus MC-University Medical Center , Rotterdam , the Netherlands.
Qiuwei Pana Department of Gastroenterology and Hepatology , Erasmus MC-University Medical Center , Rotterdam , the Netherlands.
Erasmus MC · NLChinese Academy of Agricultural Sciences · CNUniversitas Gadjah Mada · ID

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis E virus (HEV) infection is a major cause of acute hepatitis but also provokes chronic infection in immunocompromised patients. Although the pathogenesis and treatment outcome involve complex interplay between the virus and host, the nature of adaptive responses of HEV to the host immune system remain obscure at best. In this study, we used large-scale proteomic bioinformatics to profile characteristic mutations in human HEV isolates associated to ribavirin treatment failure, chronic hepatitis, hepatic failure or altered immunoreactivity. The prevalence of specific mutations was examined in a large number of protein sequences of ORF1 and ORF2 regions of the 3 major human-derived HEV genotypes (1, 3 and 4). By analyzing potential B, CD4+ and CD8+ T cell epitopes, we found that many of these mutations overlap with the predicted epitopes and are frequently present among the 3 HEV genotypes. These overlapping mutations mediate reduced antigenicity. Finally, by delineation of diversification and evolution of the underlying epitopes, we observe that most of these variants apparently evolved earlier in genotype 1 when compared with genotypes 3 and 4. These results indicate that HEV is under substantial evolutionary pressure to develop mutations enabling evasion of the host immune response and resistance to antiviral treatment. This indicates the existence of an ongoing evolutionary arms race between human immunity, antiviral medication and HEV.

Indexed as

Evolution, MolecularGenotypeAdaptation, PhysiologicalAntigenic VariationDatabases, GeneticEpitopesHepatitis EHepatitis E virusHumansMutationMutation, MissensePolymorphism, Single NucleotideProtein StabilityProteomicsViral ProteinsEpitopesViral ProteinsB and T cellsepitopeevolutionhepatitis E virusmutation

Identifiers

PMID28727933
PMCPMC5955438
OpenAlexW2736952385

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.