ArticleVirology journal2018
Substitution of amino acid residue V1213 in the helicase domain of the genotype 3 hepatitis E virus reduces virus replication.
Article in Virology journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- 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 · 2026Article
- HEV replication is promoted by blocking the NF-κB signaling pathway through inhibiting FLNa expression.Journal of virology · 2026Article
- Viral Replicon Systems and Their Biosafety Aspects.Applied biosafety : journal of the American Biological Safety Association · 2023Review
- Expanding the Hepatitis E Virus Toolbox: Selectable Replicons and Recombinant Reporter Genomes.Viruses · 2023Review
- Structural aspects of hepatitis E virus.Archives of virology · 2022Review
- Hepatitis E genotype 3 genome: A comprehensive analysis of entropy, motif conservation, relevant mutations, and clade-associated polymorphisms.Frontiers in microbiology · 2022Article
- An in silico approach to analyze HCV genotype-specific binding-site variation and its effect on drug-protein interaction.Scientific reports · 2020Article
- Coelenterazine-Dependent Luciferases as a Powerful Analytical Tool for Research and Biomedical Applications.International journal of molecular sciences · 2020Review
- Hepatitis E Virus Replication.Viruses · 2019Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundGenotype 3 hepatitis E virus (HEV) infection is generally associated with mild disease. However, recently eight genotype 3 HEV isolates were identified from patients with severe hepatitis. Importantly, three mutations (S605P, I978V and V1213A) in these genotype 3 isolates were found to be typical of genotype 4 HEV, which is sometime associated with more severe hepatitis. Therefore in this study we seek to determine if these unique mutations contribute to enhanced virus replication and thus potentially severe disease.
methodsIn the lack of an efficient cell culture system to study the effect of mutations on HEV replication, we developed a genotype 3 HEV replicon with Renilla luciferase (Rluc) as reporter and subsequently used it to construct numerous mutants, including swMu-1 (V1213A), swMu-2 (Q1246H), swMu-3 (V1213A and Q1246H), swMu-4 (S605P and I978V), and swMu-5 (V1213A, S605P and I978V). RNA transcripts from mutant replicons were transfected into Huh7 S10-3 liver cells to measure the effect of mutations on HEV replication efficiency.
resultsThe results showed that the V1213A mutant had the highest reduction in HEV replication efficiency than other mutants. The V1213A and S605P + I978V mutations have a cumulative, if not synergistic, effect on HEV replication. The Q1246H mutant decreased HEV replication compared to the wild-type HEV Rluc replicon but replicated better than the V1213A mutant. The amino acid residue V1213 favors the replication of both genotypes 3 and 4 HEV strains, but not genotype 1 HEV.
conclusionThe results suggested that the V1213A mutation reduced HEV replication, but is likely not associated with the reported severe hepatitis caused by genotype 3 HEV isolates containing this mutation.
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