ArticlePloS one2012
ARF1 and GBF1 generate a PI4P-enriched environment supportive of hepatitis C virus replication.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
45 citing papers in PubMed.
- Phosphoinositides in membrane remodeling during infections and cellular stresses.FEBS letters · 2026Review
- Inositol metabolism as a broad-spectrum antiviral target.Frontiers in microbiology · 2025Review
- Mechanism, structural and functional insights into nidovirus-induced double-membrane vesicles.Frontiers in immunology · 2024Review
- Picornavirus 3C Proteins Intervene in Host Cell Processes through Proteolysis and Interactions with RNA.Viruses · 2023Review
- The host-targeting compound peruvoside has a broad-spectrum antiviral activity against positive-sense RNA viruses.Acta pharmaceutica Sinica. B · 2023Article
- ARF1 with Sec7 Domain-Dependent GBF1 Activates Coatomer Protein I To Support Classical Swine Fever Virus Entry.Journal of virology · 2022Article
- Regulatory Role of Phospholipids in Hepatitis C Virus Replication and Protein Function.Pathogens (Basel, Switzerland) · 2022Review
- Structural and functional analysis of the small GTPase ARF1 reveals a pivotal role of its GTP-binding domain in controlling of the generation of viral inclusion bodies and replication of grass carp reovirus.Frontiers in immunology · 2022Article
- Review
- Cellular factors involved in the hepatitis C virus life cycle.World journal of gastroenterology · 2021Review
- Role of the Guanine Nucleotide Exchange Factor GBF1 in the Replication of RNA Viruses.Viruses · 2020Review
- Recent advances on the role of host factors during non-poliovirus enteroviral infections.Journal of biomedical science · 2019Review
- Functional and Physical Interaction between the Arf Activator GBF1 and Hepatitis C Virus NS3 Protein.Journal of virology · 2019Article
- Viral journeys on the intracellular highways.Cellular and molecular life sciences : CMLS · 2018Review
- Hijacking of multiple phospholipid biosynthetic pathways and induction of membrane biogenesis by a picornaviral 3CD protein.PLoS pathogens · 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
- Hepatitis C virus triggers Golgi fragmentation and autophagy through the immunity-related GTPase M.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Foot-and-mouth disease virus genome replication is unaffected by inhibition of type III phosphatidylinositol-4-kinases.The Journal of general virology · 2016Article
- Fat(al) attraction: Picornaviruses Usurp Lipid Transfer at Membrane Contact Sites to Create Replication Organelles.Trends in microbiology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Cellular levels of phosphatidylinositol 4-phosphate (PI4P) have been shown to be upregulated during RNA replication of several viruses, including the HCV replicon model. However, whether PI4P is required in an infectious HCV model remains unknown. Moreover, it is not established whether the host transport machinery is sequestered by the generation of PI4P during HCV infection. Here we found that PI4P was enriched in HCV replication complexes when Huh7.5.1 cells were infected with JFH1. HCV replication was inhibited upon overexpression of the PI4P phosphatase Sac1. The PI4P kinase PI4KIIIβ was also found to be required for HCV replication. Moreover, the vesicular transport proteins ARF1 and GBF1 colocalized with PI4KIIIβ and were both required for HCV replication. During authentic HCV infection, PI4P plays an integral role in virus replication.
Indexed as
Identifiers
What OpenQuestion holds
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.