ArticlePLoS pathogens2018
A protein coevolution method uncovers critical features of the Hepatitis C Virus fusion mechanism.
Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Different mechanisms for human rhinovirus survival in the presence of deleterious amino acid substitutions at virion protein-protein or RNA-protein interfaces.Journal of virology · 2026Article
- Hepatitis C virus E1 protein-specific linear B-cell epitopes, pan-genotype reactivity, and functional relevance.Frontiers in immunology · 2026Article
- A sequence-based evolutionary distance method for Phylogenetic analysis of highly divergent proteins.Scientific reports · 2023Article
- Article
- Secretory glycoprotein NS1 plays a crucial role in the particle formation of flaviviruses.PLoS pathogens · 2022Article
- Sites of vulnerability in HCV E1E2 identified by comprehensive functional screening.Cell reports · 2022Article
- Can next-generation humanized mice that reconstituted with both functional human immune system and hepatocytes model the progression of viral hepatitis to hepatocarcinogenesis?Frontiers in medicine · 2022Review
- Viral Causality of Human Cancer and Potential Roles of Human Endogenous Retroviruses in the Multi-Omics Era: An Evolutionary Epidemiology Review.Frontiers in oncology · 2021Review
- Identification and Characteristics of Fusion Peptides Derived From Enveloped Viruses.Frontiers in chemistry · 2021Review
- Chlorcyclizine Inhibits Viral Fusion of Hepatitis C Virus Entry by Directly Targeting HCV Envelope Glycoprotein 1.Cell chemical biology · 2020Article
- COVTree: Coevolution in OVerlapped sequences by Tree analysis server.Nucleic acids research · 2020Article
- Hepatitis C Virus Entry: An Intriguingly Complex and Highly Regulated Process.International journal of molecular sciences · 2020Review
- Flexibility and intrinsic disorder are conserved features of hepatitis C virus E2 glycoprotein.PLoS computational biology · 2020Article
- Coevolution analysis of amino-acids reveals diversified drug-resistance solutions in viral sequences: a case study of hepatitis B virus.Virus evolution · 2020Article
- Disease-relevant mutations alter amino acid co-evolution networks in the second nucleotide binding domain of CFTR.PloS one · 2020Article
- Functional expression and characterization of the envelope glycoprotein E1E2 heterodimer of hepatitis C virus.PLoS pathogens · 2019Article
- Simultaneous Bayesian inference of phylogeny and molecular coevolution.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- CoevDB: a database of intramolecular coevolution among protein-coding genes of the bony vertebrates.Nucleic acids research · 2019Article
- Role of Hepatitis C Virus Envelope Glycoprotein E1 in Virus Entry and Assembly.Frontiers in immunology · 2018Review
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20 authors.
Funding
Abstract
Amino-acid coevolution can be referred to mutational compensatory patterns preserving the function of a protein. Viral envelope glycoproteins, which mediate entry of enveloped viruses into their host cells, are shaped by coevolution signals that confer to viruses the plasticity to evade neutralizing antibodies without altering viral entry mechanisms. The functions and structures of the two envelope glycoproteins of the Hepatitis C Virus (HCV), E1 and E2, are poorly described. Especially, how these two proteins mediate the HCV fusion process between the viral and the cell membrane remains elusive. Here, as a proof of concept, we aimed to take advantage of an original coevolution method recently developed to shed light on the HCV fusion mechanism. When first applied to the well-characterized Dengue Virus (DENV) envelope glycoproteins, coevolution analysis was able to predict important structural features and rearrangements of these viral protein complexes. When applied to HCV E1E2, computational coevolution analysis predicted that E1 and E2 refold interdependently during fusion through rearrangements of the E2 Back Layer (BL). Consistently, a soluble BL-derived polypeptide inhibited HCV infection of hepatoma cell lines, primary human hepatocytes and humanized liver mice. We showed that this polypeptide specifically inhibited HCV fusogenic rearrangements, hence supporting the critical role of this domain during HCV fusion. By combining coevolution analysis and in vitro assays, we also uncovered functionally-significant coevolving signals between E1 and E2 BL/Stem regions that govern HCV fusion, demonstrating the accuracy of our coevolution predictions. Altogether, our work shed light on important structural features of the HCV fusion mechanism and contributes to advance our functional understanding of this process. This study also provides an important proof of concept that coevolution can be employed to explore viral protein mediated-processes, and can guide the development of innovative translational strategies against challenging human-tropic viruses.
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