ArticleJournal of virology2004
The poliovirus replication machinery can escape inhibition by an antiviral drug that targets a host cell protein.
Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 54 citations in OpenAlex.
- Infection-specific long-chain fatty acid metabolism as a broad anti-enterovirus target.bioRxiv : the preprint server for biology · 2026Article
- Genotype-by-inhibitor interactions to dissect enterovirus replication.Nature communications · 2026Article
- Genotype-by-Inhibitor Interactions to Dissect Enterovirus Replication.Research square · 2025Article
- Article
- Non-lytic spread of poliovirus requires the nonstructural protein 3CD.bioRxiv : the preprint server for biology · 2024Article
- 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
- Article
- High-Order Epistasis and Functional Coupling of Infection Steps Drive Virus Evolution toward Independence from a Host Pathway.Microbiology spectrum · 2021Article
- Picornaviruses: A View from 3A.Viruses · 2021Review
- Enterovirus Replication Organelles and Inhibitors of Their Formation.Frontiers in microbiology · 2020Review
- Article
- Crystal structure of a soluble fragment of poliovirus 2CATPase.PLoS pathogens · 2018Article
- The Amino Acid Substitution Q65H in the 2C Protein of Swine Vesicular Disease Virus Confers Resistance to Golgi Disrupting Drugs.Frontiers in microbiology · 2016Article
- Review
- Cell-specific establishment of poliovirus resistance to an inhibitor targeting a cellular protein.Journal of virology · 2015Article
- Article
- Picornavirus--host interactions to construct viral secretory membranes.Progress in molecular biology and translational science · 2015Review
- Poliovirus-induced changes in cellular membranes throughout infection.Current opinion in virology · 2014Review
- New small-molecule inhibitors effectively blocking picornavirus replication.Journal of virology · 2014Article
- Rewiring of cellular membrane homeostasis by picornaviruses.Journal of virology · 2014Review
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
Viral replication depends on specific interactions with host factors. For example, poliovirus RNA replication requires association with intracellular membranes. Brefeldin A (BFA), which induces a major rearrangement of the cellular secretory apparatus, is a potent inhibitor of poliovirus RNA replication. Most aspects governing the relationship between viral replication complex and the host membranes remain poorly defined. To explore these interactions, we used a genetic approach and isolated BFA-resistant poliovirus variants. Mutations within viral proteins 2C and 3A render poliovirus resistant to BFA. In the absence of BFA, viruses containing either or both of these mutations replicated similarly to wild type. In the presence of BFA, viruses carrying a single mutation in 2C or 3A exhibited an intermediate-growth phenotype, while the double mutant was fully resistant. The viral proteins 2C and 3A have critical roles in both RNA replication and vesicle formation. The identification of BFA resistant mutants may facilitate the identification of cellular membrane-associated proteins necessary for induction of vesicle formation and RNA replication. Importantly, our data underscore the dramatic plasticity of the host-virus interactions required for successful viral 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.