Evidence map›Paper›PMID 38712945›Full record

ArticleJournal of virology2024

Characterization of virus‒host recombinant variants of the hepatitis E virus.

Olivia Paronetto, Claire Allioux, Chloé Diméglio, Lhorane Lobjois, Nicolas Jeanne, Noémie Ranger, Jérôme Boineau, Mélanie Pucelle, Sofia Demmou, Florence Abravanel and 3 more

Abstract read
In one paragraph

Article in Journal of virology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Proteasomal processing of the viral replicase ORF1 facilitates HEV-induced liver fibrosis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Article
  7. 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

13 authors.

Olivia ParonettoInstitut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity), UMR 5051 (CNRS), UMR 1291 (INSERM), Université Toulouse III-Paul Sabatier, Toulouse, France.ORCID 0009-0007-1788-549X
Claire AlliouxInstitut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity), UMR 5051 (CNRS), UMR 1291 (INSERM), Université Toulouse III-Paul Sabatier, Toulouse, France.
Chloé DiméglioInstitut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity), UMR 5051 (CNRS), UMR 1291 (INSERM), Université Toulouse III-Paul Sabatier, Toulouse, France.
Lhorane LobjoisInstitut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity), UMR 5051 (CNRS), UMR 1291 (INSERM), Université Toulouse III-Paul Sabatier, Toulouse, France.
Nicolas JeanneInstitut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity), UMR 5051 (CNRS), UMR 1291 (INSERM), Université Toulouse III-Paul Sabatier, Toulouse, France.
Noémie RangerLaboratoire de Virologie, Hôpital Purpan, CHU Toulouse, Toulouse, France.
Jérôme BoineauLaboratoire de Virologie, Hôpital Purpan, CHU Toulouse, Toulouse, France.
Mélanie PucelleLaboratoire de Virologie, Hôpital Purpan, CHU Toulouse, Toulouse, France.
Sofia DemmouLaboratoire de Virologie, Hôpital Purpan, CHU Toulouse, Toulouse, France.
Florence AbravanelInstitut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity), UMR 5051 (CNRS), UMR 1291 (INSERM), Université Toulouse III-Paul Sabatier, Toulouse, France.
Sabine Chapuy-RegaudInstitut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity), UMR 5051 (CNRS), UMR 1291 (INSERM), Université Toulouse III-Paul Sabatier, Toulouse, France.
Jacques IzopetInstitut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity), UMR 5051 (CNRS), UMR 1291 (INSERM), Université Toulouse III-Paul Sabatier, Toulouse, France.ORCID 0000-0002-8462-3234
Sébastien LhommeInstitut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity), UMR 5051 (CNRS), UMR 1291 (INSERM), Université Toulouse III-Paul Sabatier, Toulouse, France.ORCID 0000-0001-7908-1576

Funding

Agence Nationale de Recherches sur le Sida et les Hépatites Virales (ANRS) ECTZ159924Agence Nationale de Recherches sur le Sida et les Hépatites Virales (ANRS) ECTZ189528
6 · The paper itself

Abstract

Hepatitis E virus is a single-strand, positive-sense RNA virus that can lead to chronic infection in immunocompromised patients. Virus-host recombinant variants (VHRVs) have been described in such patients. These variants integrate part of human genes into the polyproline-rich region that could introduce new post-translational modifications (PTMs), such as ubiquitination. The aim of this study was to characterize the replication capacity of different VHRVs, namely, RNF19A, ZNF787, KIF1B, EEF1A1, RNA18, RPS17, and RPL6. We used a plasmid encoding the Kernow strain, in which the fragment encoding the S17 insertion was deleted (Kernow p6 delS17) or replaced by fragments encoding the different insertions. The HEV RNA concentrations in the supernatants and the HepG2/C3A cell lysates were determined via RT-qPCR. The capsid protein ORF2 was immunostained. The effect of ribavirin was also assessed. The HEV RNA concentrations in the supernatants and the cell lysates were higher for the variants harboring the RNF19A, ZNF787, KIF1B, RPS17, and EEF1A1 insertions than for the Kernow p6 del S17, while it was not with RNA18 or RPL6 fragments. The number of ORF2 foci was higher for RNF19A, ZNF787, KIF1B, and RPS17 than for Kernow p6 del S17. VHRVs with replicative advantages were less sensitive to the antiviral effect of ribavirin. No difference in PTMs was found between VHRVs with a replicative advantage and those without. In conclusion, our study showed that insertions did not systematically confer a replicative advantage IMPORTANCE: Hepatitis E virus (HEV) is a major cause of viral hepatitis. HEV can lead to chronic infection in immunocompromised patients. Ribavirin treatment is currently used to treat such chronic infections. Recently, seven virus-host recombinant viruses were characterized in immunocompromised patients. These viruses have incorporated a portion of a human gene fragment into their genome. We studied the consequences of these insertions on the replication capacity. We found that these inserted fragments could enhance virus replication for five of the seven recombinant variants. We also showed that the recombinant variants with replicative advantages were less sensitive to ribavirin

Indexed as

Hepatitis E virusHost Microbial InteractionsRecombination, GeneticAntiviral AgentsHepatitis EHep G2 CellsHumansPlasmidsProtein Processing, Post-TranslationalRibavirinRNA, ViralUbiquitinationViral ProteinsVirus ReplicationAntiviral AgentsORF2 protein, Hepatitis E virusRibavirinRNA, ViralViral Proteinshepatitis E virusribavirinviral fitnessvirus–host recombinant variants

Identifiers

PMID38712945
PMCPMC11237545

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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.