Evidence map›Paper›PMID 22837418›Full record

ArticleThe Journal of general virology2012

Evolution of the hepatitis E virus hypervariable region.

Donald B Smith, Jeff Vanek, Sandeep Ramalingam, Ingolfur Johannessen, Kate Templeton, Peter Simmonds

Open access · hybridAbstract read
In one paragraph

Article in The Journal of general virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Genetic Evolution of Hepatitis E Virus.Advances in experimental medicine and biology · 2023
    Review
  5. Hepatitis E Virus Life Cycle.Advances in experimental medicine and biology · 2023
    Article
  6. Structural aspects of hepatitis E virus.Archives of virology · 2022
    Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Life cycle and morphogenesis of the hepatitis E virus.Emerging microbes & infections · 2018
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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 2 institutions in 1 country.

Donald B SmithCentre for Immunity, Infection and Evolution, University of Edinburgh, Ashworth Building, King's Buildings, Edinburgh EH9 3JF, UK.
Jeff VanekDepartment of Laboratory Medicine, Royal Infirmary of Edinburgh, Little France, Edinburgh EH16 4SA, UK.
Sandeep RamalingamDepartment of Laboratory Medicine, Royal Infirmary of Edinburgh, Little France, Edinburgh EH16 4SA, UK.
Ingolfur JohannessenDepartment of Laboratory Medicine, Royal Infirmary of Edinburgh, Little France, Edinburgh EH16 4SA, UK.
Kate TempletonDepartment of Laboratory Medicine, Royal Infirmary of Edinburgh, Little France, Edinburgh EH16 4SA, UK.
Peter SimmondsCentre for Immunity, Infection and Evolution, University of Edinburgh, Ashworth Building, King's Buildings, Edinburgh EH9 3JF, UK.
Edinburgh Royal Infirmary · GBUniversity of Edinburgh · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

The presence of a hypervariable (HVR) region within the genome of hepatitis E virus (HEV) remains unexplained. Previous studies have described the HVR as a proline-rich spacer between flanking functional domains of the ORF1 polyprotein. Others have proposed that the region has no function, that it reflects a hypermutable region of the virus genome, that it is derived from the insertion and evolution of host sequences or that it is subject to positive selection. This study attempts to differentiate between these explanations by documenting the evolutionary processes occurring within the HVR. We have measured the diversity of HVR sequences within acutely infected individuals or amongst sequences derived from epidemiologically linked samples and, surprisingly, find relative homogeneity amongst these datasets. We found no evidence of positive selection for amino acid substitution in the HVR. Through an analysis of published sequences, we conclude that the range of HVR diversity observed within virus genotypes can be explained by the accumulation of substitutions and, to a much lesser extent, through deletions or duplications of this region. All published HVR amino acid sequences display a relative overabundance of proline and serine residues that cannot be explained by a local bias towards cytosine in this part of the genome. Although all published HVRs contain one or more SH3-binding PxxP motifs, this motif does not occur more frequently than would be expected from the proportion of proline residues in these sequences. Taken together, these observations are consistent with the hypothesis that the HVR has a structural role that is dependent upon length and amino acid composition, rather than a specific sequence.

Indexed as

Genome, ViralAdultAgedAmino Acid SequenceFemaleGene Expression Regulation, ViralHepatitis EHepatitis E virusHumansMaleMiddle AgedMolecular Sequence DataViral ProteinsORF2 protein, Hepatitis E virusViral Proteins

Identifiers

PMID22837418
PMCPMC3542125
OpenAlexW2129543078

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.