ArticlePLoS pathogens2017
Hepatitis E virus persists in the presence of a type III interferon response.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 93 citations in OpenAlex.
- Host-interferon-stimulated gene response to virus-host recombinant variants of hepatitis E virus and enhanced viral replication.Microbiology spectrum · 2026Article
- The evolution of in vitro culture systems for the study of hepatitis E virus infection.Virology · 2026Review
- Exacerbation of Anti-Cytomegalovirus Immunity and Mobilization of γ9δ1 T Cells During the Acute Phase of Hepatitis E Virus Infection.Microbiology and immunology · 2026Article
- GRP75 blocks hepatitis E virus infection by targeting HEV-ORF2 for degradation through chaperone-mediated autophagy and promoting IRF3 activation.Journal of virology · 2026Article
- Mitochondrial and lipid metabolism rewiring during HEV infection.Cellular and molecular life sciences : CMLS · 2026Article
- Virological and immunological determinants of hepatitis E virus infection outcomes.Current opinion in virology · 2025Review
- The hepatitis E virus capsid protein ORF2 counteracts cell-intrinsic antiviral responses to enable persistent replication in cell culture.PLoS pathogens · 2025Article
- Plasmacytoid dendritic cell sensing of hepatitis E virus is shaped by both viral and host factors.Life science alliance · 2025Article
- Trends and Challenges in the Detection and Environmental Surveillance of the Hepatitis E Virus.Microorganisms · 2025Review
- Hepatitis E virus: from innate sensing to adaptive immune responses.Nature reviews. Gastroenterology & hepatology · 2024Review
- From discovery to treatment: tracing the path of hepatitis E virus.Virology journal · 2024Review
- Characterization of virus‒host recombinant variants of the hepatitis E virus.Journal of virology · 2024Article
- Tripartite Motif-Containing Protein 65 (TRIM65) Inhibits Hepatitis B Virus Transcription.Viruses · 2024Article
- Review
- miR-26a exerts broad-spectrum antiviral effects via the enhancement of RIG-I-mediated type I interferon response by targeting USP15.Microbiology spectrum · 2024Article
- Virus-Host Protein Interaction Network of the Hepatitis E Virus ORF2-4 by Mammalian Two-Hybrid Assays.Viruses · 2023Article
- Hepatitis E Virus Infections: Epidemiology, Genetic Diversity, and Clinical Considerations.Viruses · 2023Review
- Immunobiology and Host Response to HEV.Advances in experimental medicine and biology · 2023Article
- Identification of interferon-stimulated genes with modulated expression during hepatitis E virus infection in pig liver tissues and human HepaRG cells.Frontiers in immunology · 2023Article
- Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The RIG-I-like RNA helicase (RLR)-mediated interferon (IFN) response plays a pivotal role in the hepatic antiviral immunity. The hepatitis A virus (HAV) and the hepatitis C virus (HCV) counter this response by encoding a viral protease that cleaves the mitochondria antiviral signaling protein (MAVS), a common signaling adaptor for RLRs. However, a third hepatotropic RNA virus, the hepatitis E virus (HEV), does not appear to encode a functional protease yet persists in infected cells. We investigated HEV-induced IFN responses in human hepatoma cells and primary human hepatocytes. HEV infection resulted in persistent virus replication despite poor spread. This was companied by a type III IFN response that upregulated multiple IFN-stimulated genes (ISGs), but type I IFNs were barely detected. Blocking type III IFN production or signaling resulted in reduced ISG expression and enhanced HEV replication. Unlike HAV and HCV, HEV did not cleave MAVS; MAVS protein size, mitochondrial localization, and function remained unaltered in HEV-replicating cells. Depletion of MAVS or MDA5, and to a less extent RIG-I, also diminished IFN production and increased HEV replication. Furthermore, persistent activation of the JAK/STAT signaling rendered infected cells refractory to exogenous IFN treatment, and depletion of MAVS or the receptor for type III IFNs restored the IFN responsiveness. Collectively, these results indicate that unlike other hepatotropic RNA viruses, HEV does not target MAVS and its persistence is associated with continuous production of type III IFNs.
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