ArticleJournal of virology2014
Hepatitis C virus NS5A hijacks ARFGAP1 to maintain a phosphatidylinositol 4-phosphate-enriched microenvironment.
Article in Journal of virology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 48 citations in OpenAlex.
- ARFGAP1 serves as a critical host factor during E30 infection: QS11 inhibits viral pathogenesis in hFcRn-IFNARVirology journal · 2025Article
- COP I vesicles facilitate classical swine fever virus proliferation by transporting fatty acid synthase from the Golgi apparatus to the endoplasmic reticulum.Journal of virology · 2025Article
- The emerging roles of retromer and sorting nexins in the life cycle of viruses.Virologica Sinica · 2022Review
- Regulatory Role of Phospholipids in Hepatitis C Virus Replication and Protein Function.Pathogens (Basel, Switzerland) · 2022Review
- Cytoplasmic tail determines the membrane trafficking and localization of SARS-CoV-2 spike protein.Frontiers in molecular biosciences · 2022Review
- Role of the Guanine Nucleotide Exchange Factor GBF1 in the Replication of RNA Viruses.Viruses · 2020Review
- Emerging Role for Acyl-CoA Binding Domain Containing 3 at Membrane Contact Sites During Viral Infection.Frontiers in microbiology · 2020Review
- Elucidating the Host Interactome of EV-A71 2C Reveals Viral Dependency Factors.Frontiers in microbiology · 2019Article
- Viral journeys on the intracellular highways.Cellular and molecular life sciences : CMLS · 2018Review
- NAP1L1 Regulates Hepatitis C Virus Entry and Interacts with NS3.Virologica Sinica · 2018Article
- Interplay between hepatitis C virus and ARF4.Virologica Sinica · 2017Article
- Protein Inhibitor of Activated STAT2 Restricts HCV Replication by Modulating Viral Proteins Degradation.Viruses · 2017Article
- Sec24C-Dependent Transport of Claudin-1 Regulates Hepatitis C Virus Entry.Journal of virology · 2017Article
- Retromer localizes to autophagosomes during HCV replication.Virologica Sinica · 2017Article
- Bioinformatics analysis of the proteins interacting with LASP-1 and their association with HBV-related hepatocellular carcinoma.Scientific reports · 2017Article
- Hepatitis C virus NS5A protein cooperates with phosphatidylinositol 4-kinase IIIα to induce mitochondrial fragmentation.Scientific reports · 2016Article
- A role for retromer in hepatitis C virus replication.Cellular and molecular life sciences : CMLS · 2016Article
- Host restriction factors for hepatitis C virus.World journal of gastroenterology · 2016Review
- HCV and Oxidative Stress: Implications for HCV Life Cycle and HCV-Associated Pathogenesis.Oxidative medicine and cellular longevity · 2016Review
- Riding the R Train into the Cell.PLoS pathogens · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
unlabelledPhosphatidylinositol 4-phosphate (PI4P) is well known to be upregulated during hepatitis C virus (HCV) replication. The role of PI4 kinases in HCV has been extensively investigated. Whether the PI4P phosphatase Sac1 is altered by HCV remains unclear. Here, we identified ARFGAP1 to be a novel host factor for HCV replication. We further show that Sac1 interacts with ARFGAP1 and inhibits HCV replication. The elevation of PI4P induced by HCV NS5A is abrogated when the coatomer protein I (COPI) pathway is inhibited. We also found an interaction between NS5A and ARFGAP1. Furthermore, we identified a conserved cluster of positively charged amino acids in NS5A critical for interaction between NS5A and ARFGAP1, induction of PI4P, and HCV replication. Our data demonstrate that ARFGAP1 is a host factor for HCV RNA replication. ARFGAP1 is hijacked by HCV NS5A to remove COPI cargo Sac1 from the site of HCV replication to maintain high levels of PI4P. Our findings provide an additional mechanism by which HCV enhances formation of a PI4P-rich environment. IMPORTANCE: PI4P is enriched in the replication area of HCV; however, whether PI4P phosphatase Sac1 is subverted by HCV is not established. The detailed mechanism of how COPI contributes to viral replication remains unknown, though COPI components were hijacked by HCV. We demonstrate that ARFGAP1 is hijacked by HCV NS5A to remove COPI cargo Sac1 from the HCV replication area to maintain high-level PI4P generated by NS5A. Furthermore, we identify a conserved cluster of positively charged amino acids in NS5A, which are critical for interaction between NS5A and ARFGAP1, induction of PI4P, and HCV replication. This study will shed mechanistic insight on how other RNA viruses hijack COPI and Sac1.
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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.