ArticleJournal of virology2011
NS4B self-interaction through conserved C-terminal elements is required for the establishment of functional hepatitis C virus replication complexes.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed.
- Deciphering the membrane topology of the pestiviral non-structural protein 4B (NS4B).Journal of virology · 2025Article
- Modes of action of a small molecule antiviral compound targeting yellow fever virus NS4B protein.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Endosomal egress and intercellular transmission of hepatic ApoE-containing lipoproteins and its exploitation by the hepatitis C virus.PLoS pathogens · 2023Article
- A new host-targeted antiviral cyclolignan (SAU-22.107) for Dengue Virus infection in cell cultures. Potential action mechanisms based on cell imaging.Virus research · 2023Article
- Characterization of a multipurpose NS3 surface patch coordinating HCV replicase assembly and virion morphogenesis.PLoS pathogens · 2022Article
- Contribution of autophagy machinery factors to HCV and SARS-CoV-2 replication organelle formation.Cell reports · 2021Article
- Life cycle process dependencies of positive-sense RNA viruses suggest strategies for inhibiting productive cellular infection.Journal of the Royal Society, Interface · 2021Article
- Determinants in Nonstructural Protein 4A of Dengue Virus Required for RNA Replication and Replication Organelle Biogenesis.Journal of virology · 2021Article
- Review
- Live-Cell Analysis of Human Cytomegalovirus DNA Polymerase Holoenzyme Assembly by Resonance Energy Transfer Methods.Microorganisms · 2021Article
- Hepatitis C Viral Replication Complex.Viruses · 2021Review
- Comparative Analysis of Hepatitis C Virus NS5A Dynamics and Localization in Assembly-Deficient Mutants.Pathogens (Basel, Switzerland) · 2021Article
- Double-Membrane Vesicles as Platforms for Viral Replication.Trends in microbiology · 2020Review
- The bZIP Proteins of Oncogenic Viruses.Viruses · 2020Review
- Proton-Detected Solid-State NMR of the Cell-Free Synthesized α-Helical Transmembrane Protein NS4B from Hepatitis C Virus.Chembiochem : a European journal of chemical biology · 2020Article
- Hepatitis C Virus Replication.Cold Spring Harbor perspectives in medicine · 2020Review
- Determination of Critical Requirements for Classical Swine Fever Virus NS2-3-Independent Virion Formation.Journal of virology · 2019Article
- RACK1 mediates rewiring of intracellular networks induced by hepatitis C virus infection.PLoS pathogens · 2019Article
- Review
- HCV NS5A dimer interface residues regulate HCV replication by controlling its self-interaction, hyperphosphorylation, subcellular localization and interaction with cyclophilin A.PLoS pathogens · 2018Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis C virus (HCV) is an important human pathogen, persistently infecting more than 170 million individuals worldwide. Studies of the HCV life cycle have become possible with the development of cell culture systems supporting the replication of viral RNA and the production of infectious virus. However, the exact functions of individual proteins, especially of nonstructural protein 4B (NS4B), remain poorly understood. NS4B triggers the formation of specific, vesicular membrane rearrangements, referred to as membranous webs, which have been reported to represent sites of HCV RNA replication. However, the mechanism of vesicle induction is not known. In this study, a panel of 15 mutants carrying substitutions in the highly conserved NS4B C-terminal domain was generated. Five mutations had only a minor effect on replication, but two of them enhanced assembly and release of infectious virus. Ten mutants were replication defective and used for selection of pseudoreversions. Most of the pseudoreversions also localized to the highly conserved NS4B C-terminal domain and were found to restore replication competence upon insertion into the corresponding primary mutant. Importantly, pseudoreversions restoring replication competence also restored heterotypic NS4B self-interaction, which was disrupted by the primary mutation. Finally, electron microscopy analyses of membrane alterations induced by NS4B mutants revealed striking morphological abnormalities, which were restored to wild-type morphology by the corresponding pseudoreversion. These findings demonstrate the important role of the C-terminal domain in NS4B self-interaction and the formation of functional HCV replication complexes.
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