ArticleJournal of virology2008
NS3 helicase domains involved in infectious intracellular hepatitis C virus particle assembly.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers.
What it found
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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.
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.
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Who cites it
131 citing papers in PubMed, 194 citations in OpenAlex.
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- AlphaFold Prediction of Protein-Protein Interactions in theInternational journal of molecular sciences · 2025Article
- Hepatitis C virus NS3 helicase contributes to (-) strand RNA synthesis.Nature communications · 2025Article
- Characterization of a multipurpose NS3 surface patch coordinating HCV replicase assembly and virion morphogenesis.PLoS pathogens · 2022Article
- The Emerging Roles of Silver Nanoparticles to Target Viral Life Cycle and Detect Viral Pathogens.Chemistry, an Asian journal · 2022Review
- SPCS1-Dependent E2-p7 processing determines HCV Assembly efficiency.PLoS pathogens · 2022Article
- Epistatic interactions promote persistence of NS3-Q80K in HCV infection by compensating for protein folding instability.The Journal of biological chemistry · 2021Article
- Cellular factors involved in the hepatitis C virus life cycle.World journal of gastroenterology · 2021Review
- HCV Assembly and Egress via Modifications in Host Lipid Metabolic Systems.Cold Spring Harbor perspectives in medicine · 2021Review
- Extended interaction networks with HCV protease NS3-4A substrates explain the lack of adaptive capability against protease inhibitors.The Journal of biological chemistry · 2020Article
- Article
- An Update on African Swine Fever Virology.Viruses · 2019Review
- Preclinical evaluation of Amphihevir, a first-in-class clinical Hepatitis C virus NS4B inhibitor.Antimicrobial agents and chemotherapy · 2019Article
- Evolutionary Pathways to Persistence of Highly Fit and Resistant Hepatitis C Virus Protease Inhibitor Escape Variants.Hepatology (Baltimore, Md.) · 2019Review
- TNRC6 proteins modulate hepatitis C virus replication by spatially regulating the binding of miR-122/Ago2 complexes to viral RNA.Nucleic acids research · 2019Article
- Impact of novel NS5A resistance-associated substitutions of hepatitis C virus detected in treatment-experienced patients.Scientific reports · 2019Article
- Functional and Physical Interaction between the Arf Activator GBF1 and Hepatitis C Virus NS3 Protein.Journal of virology · 2019Article
- The acidic domain of the hepatitis C virus NS4A protein is required for viral assembly and envelopment through interactions with the viral E1 glycoprotein.PLoS pathogens · 2019Article
- Overview of HCV Life Cycle with a Special Focus on Current and Possible Future Antiviral Targets.Viruses · 2019Review
- The QP509L and Q706L superfamily II RNA helicases of African swine fever virus are required for viral replication, having non-redundant activities.Emerging microbes & infections · 2019Article
71 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
A mutation within subdomain 1 of the hepatitis C virus (HCV) NS3 helicase (NS3-Q221L) (M. Yi, Y. Ma, J. Yates, and S. M. Lemon, J. Virol. 81:629-638, 2007) rescues a defect in production of infectious virus by an intergenotypic chimeric RNA (HJ3). Although NS3-Gln-221 is highly conserved across HCV genotypes, the Leu-221 substitution had no effect on RNA replication or NS3-associated enzymatic activities. However, while transfection of unmodified HJ3 RNA failed to produce either extracellular or intracellular infectious virus, transfection of HJ3 RNA containing the Q221L substitution (HJ3/QL) resulted in rapid accumulation of intracellular infectious particles with release into extracellular fluids. In the absence of the Q221L mutation, both NS5A and NS3 were recruited to core protein on the surface of lipid droplets, but there was no assembly of core into high-density, rapidly sedimenting particles. Further analysis demonstrated that a Q221N mutation minimally rescued virus production and led to a second-site I399V mutation in subdomain 2 of the helicase. Similarly, I399V alone allowed only low-level virus production and led to selection of an I286V mutation in subdomain 1 of the helicase which fully restored virus production, confirming the involvement of both major helicase subdomains in the assembly process. Thus, multiple mutations in the helicase rescue a defect in an early-intermediate step in virus assembly that follows the recruitment of NS5A to lipid droplets and precedes the formation of dense intracellular viral particles. These data reveal a previously unsuspected role for the NS3 helicase in early virion morphogenesis and provide a new perspective on HCV assembly.
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Registered trials
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.