ArticleCellular microbiology2018
Identification of GBF1 as a cellular factor required for hepatitis E virus RNA replication.
Article in Cellular microbiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Article
- The AP-1 adaptor complex is essential for intracellular trafficking of the ORF2 capsid protein and assembly of Hepatitis E virus.Cellular and molecular life sciences : CMLS · 2024Article
- A genome-wide CRISPR/Cas9 screen identifies a role for Rab5A and early endosomes in hepatitis E virus replication.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- The development of resistance to an inhibitor of a cellular protein reveals a critical interaction between the enterovirus protein 2C and a small GTPase Arf1.PLoS pathogens · 2023Article
- Viral protein engagement of GBF1 induces host cell vulnerability through synthetic lethality.The Journal of cell biology · 2022Article
- A Proximity biotinylation assay with a host protein bait reveals multiple factors modulating enterovirus replication.PLoS pathogens · 2022Article
- AG1478 Elicits a Novel Anti-Influenza Function via an EGFR-Independent, GBF1-Dependent Pathway.International journal of molecular sciences · 2022Article
- Rab1b-GBF1-ARF1 Secretory Pathway Axis Is Required for Birnavirus Replication.Journal of virology · 2022Article
- Processing and Subcellular Localization of the Hepatitis E Virus Replicase: Identification of Candidate Viral Factories.Frontiers in microbiology · 2022Article
- Hepatitis E Virus Immunopathogenesis.Pathogens (Basel, Switzerland) · 2021Review
- Advances in Hepatitis E Virus Biology and Pathogenesis.Viruses · 2021Review
- Enterovirus Infection Induces Massive Recruitment of All Isoforms of Small Cellular Arf GTPases to the Replication Organelles.Journal of virology · 2020Article
- Viral protein engagement of GBF1 induces host cell vulnerability through synthetic lethality.bioRxiv : the preprint server for biology · 2020Article
- Role of the Guanine Nucleotide Exchange Factor GBF1 in the Replication of RNA Viruses.Viruses · 2020Review
- Review
- Quantitative Proteomics of Uukuniemi Virus-host Cell Interactions Reveals GBF1 as Proviral Host Factor for Phleboviruses.Molecular & cellular proteomics : MCP · 2019Article
- A Redundant Mechanism of Recruitment Underlies the Remarkable Plasticity of the Requirement of Poliovirus Replication for the Cellular ArfGEF GBF1.Journal of virology · 2019Article
- Recombinant Hepatitis E Viruses Harboring Tags in the ORF1 Protein.Journal of virology · 2019Article
- A GBF1-Dependent Mechanism for Environmentally Responsive Regulation of ER-Golgi Transport.Developmental cell · 2019Article
- Functional and Physical Interaction between the Arf Activator GBF1 and Hepatitis C Virus NS3 Protein.Journal of virology · 2019Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The hepatitis E virus (HEV) genome is a single-stranded, positive-sense RNA that encodes three proteins including the ORF1 replicase. Mechanisms of HEV replication in host cells are unclear, and only a few cellular factors involved in this step have been identified so far. Here, we used brefeldin A (BFA) that blocks the activity of the cellular Arf guanine nucleotide exchange factors GBF1, BIG1, and BIG2, which play a major role in reshuffling of cellular membranes. We showed that BFA inhibits HEV replication in a dose-dependent manner. The use of siRNA and Golgicide A identified GBF1 as a host factor critically involved in HEV replication. Experiments using cells expressing a mutation in the catalytic domain of GBF1 and overexpression of wild type GBF1 or a BFA-resistant GBF1 mutant rescuing HEV replication in BFA-treated cells, confirmed that GBF1 is the only BFA-sensitive factor required for HEV replication. We demonstrated that GBF1 is likely required for the activity of HEV replication complexes. However, GBF1 does not colocalise with the ORF1 protein, and its subcellular distribution is unmodified upon infection or overexpression of viral proteins, indicating that GBF1 is likely not recruited to replication sites. Together, our results suggest that HEV replication involves GBF1-regulated mechanisms.
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