HEV Mutation Detail Information

Virus Mutation HEV Mutation G1634R


Basic Characteristics of Mutations
Mutation Site G1634R
Mutation Site Sentence The p6_G1634R resulted in similar infection levels compared to the wild-type strain, with the exception of mouse 6, which showed a delayed viral growth (Fig. 4).
Mutation Level Amino acid level
Mutation Type Nonsynonymous substitution
Gene/Protein/Region RdRp
Standardized Encoding Gene ORF1
Genotype/Subtype Genotype 3
Viral Reference JQ679013
Functional Impact and Mechanisms
Disease Cell line    
Immune Y
Target Gene -
Clinical and Epidemiological Correlations
Clinical Information -
Treatment Ribavirin
Location -
Literature Information
PMID 31896581
Title Robust hepatitis E virus infection and transcriptional response in human hepatocytes
Author Todt D,Friesland M,Moeller N,Praditya D,Kinast V,Bruggemann Y,Knegendorf L,Burkard T,Steinmann J,Burm R,Verhoye L,Wahid A,Meister TL,Engelmann M,Pfankuche VM,Puff C,Vondran FWR,Baumgartner W,Meuleman P,Behrendt P,Steinmann E
Journal Proceedings of the National Academy of Sciences of the United States of America
Journal Info 2020 Jan 21;117(3):1731-1741
Abstract Hepatitis E virus (HEV) is the causative agent of hepatitis E in humans and the leading cause for acute viral hepatitis worldwide. The virus is classified as a member of the genus Orthohepevirus A within the Hepeviridae family. Due to the absence of a robust cell culture model for HEV infection, the analysis of the viral life cycle, the development of effective antivirals and a vaccine is severely limited. In this study, we established a protocol based on the HEV genotype 3 p6 (Kernow C-1) and the human hepatoma cell lines HepG2 and HepG2/C3A with different media conditions to produce intracellular HEV cell culture-derived particles (HEVcc) with viral titers between 10(5) and 10(6) FFU/mL. Viral titers could be further enhanced by an HEV variant harboring a mutation in the RNA-dependent RNA polymerase. These HEVcc particles were characterized in density gradients and allowed the trans-complementation of subgenomic reporter HEV replicons. In addition, in vitro produced intracellular-derived particles were infectious in liver-humanized mice with high RNA copy numbers detectable in serum and feces. Efficient infection of primary human and swine hepatocytes using the developed protocol could be observed and was inhibited by ribavirin. Finally, RNA sequencing studies of HEV-infected primary human hepatocytes demonstrated a temporally structured transcriptional defense response. In conclusion, this robust cell culture model of HEV infection provides a powerful tool for studying viral-host interactions that should facilitate the discovery of antiviral drugs for this important zoonotic pathogen.
Sequence Data GSE135619
Mutation Information
Note
Basic Characteristics of Mutations
  • Mutation Site: The specific location in a gene or protein sequence where a change occurs.
  • Mutation Level: The level at which a mutation occurs, including the nucleotide or amino acid level.
  • Mutation Type: The nature of the mutation, such as missense mutation, nonsense mutation, synonymous mutation, etc.
  • Gene/Protein/Region: Refers to the specific region of the virus where the mutation occurs. Including viral genes, viral proteins, or a specific viral genome region. If the article does not specifically indicate the relationship between the mutation and its correspondence, the main
  • Gene/Protein/Region studied in the article is marked.
  • Genotype/Subtype: Refers to the viral genotype or subtype where the mutation occurs. If the article does not specifically indicate the relationship between the mutation and its correspondence, the main Genotype/Subtype studied in the article is marked.
  • Viral Reference: Refers to the standard virus strain used to compare and analyze viral sequences.
Functional Impact and Mechanisms
  • Disease: An abnormal physiological state with specific symptoms and signs caused by viral infection.
  • Immune: The article focuses on the study of mutations and immune.
  • Target Gene: Host genes that viral mutations may affect.
Clinical and Epidemiological Correlations
  • Clinical Information: The study is a clinical or epidemiological study and provides basic information about the population.
  • Treatment: The study mentioned a certain treatment method, such as drug resistance caused by mutations. If the study does not specifically indicate the relationship between mutations and their correspondence treatment, the main treatment studied in the article is marked.
  • Location: The source of the research data.
Literature Information
  • Sequence Data: The study provides the data accession number.