ArticleJournal of virology2010
2A protease is not a prerequisite for poliovirus replication.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
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Who cites it
10 citing papers in PubMed.
- Poliovirus 3Dpol polymerase region is essential for cleavage of poliovirus 3AB in vivo.PLoS pathogens · 2026Article
- The multifaceted role of the viral 2A protease in enterovirus replication and antagonism of host antiviral responses.PLoS pathogens · 2025Article
- An efficientJournal of virology · 2024Article
- The EV71 2A protease occupies the central cleft of SETD3 and disrupts SETD3-actin interaction.Nature communications · 2024Article
- Comprehensive Elucidation of the Role of L and 2A Security Proteins on Cell Death during EMCV Infection.Viruses · 2024Article
- Structures and Corresponding Functions of Five Types of Picornaviral 2A Proteins.Frontiers in microbiology · 2017Review
- Cytopathic effects: virus-modulated manifestations of innate immunity?Trends in microbiology · 2012Review
- Suppression of injuries caused by a lytic RNA virus (mengovirus) and their uncoupling from viral reproduction by mutual cell/virus disarmament.Journal of virology · 2012Article
- The multifaceted poliovirus 2A protease: regulation of gene expression by picornavirus proteases.Journal of biomedicine & biotechnology · 2011Article
- Viral security proteins: counteracting host defences.Nature reviews. Microbiology · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Poliovirus (PV) 2A(pro) has been considered important for PV replication and is known to be toxic to host cells. A 2A(pro)-deficient PV would potentially be less toxic and ideal as a vector. To examine whether 2A(pro) is needed to form progeny virus, a full-length cDNA of dicistronic (dc) PV with (pOME) or without (pOMEDelta2A) 2A(pro) was constructed in the strain PV1(M)OM. RNAs of both pOME and pOMEDelta2A were capable of forming progeny viruses, called OME and OMEDelta2A, respectively. In their ability to induce a cytopathic effect (CPE), the strains ranked as OMEDelta2A < OME falling dots PV1(M)OM. These results suggest that 2A(pro) is not essential for full-length dc PV to form progeny virus and that it contributes to the efficient viral replication and/or induction of a CPE. To clarify whether 2A(pro) is essential for P1-null (lacking the entire coding sequence for capsid proteins) PV, the RNA replication activity of P1-null PV (pOMDeltaP1) or P1-null PV without 2A(pro) (pOMDeltaP1Delta2A) or without both 2A(pro) and 2B (pOMDeltaP1Delta2ADelta2B) was examined. The RNAs of pOMDeltaP1 and pOMDeltaP1Delta2A could replicate and form progeny viruses under a trans supply of P1 protein, whereas the RNA of pOMDeltaP1Delta2ADelta2B could not. These results suggest that 2A(pro) is not needed for the replication of P1-null PV, although it is important for PV RNA replication and inducing a CPE. To know whether a 2A(pro)-deficient PV can be used as a vector, a P1-null PV containing the enhanced green fluorescent protein (EGFP) coding sequence with or without 2A(pro) was examined. It expressed fluorescent protein. This result suggests that 2A(pro)-deficient PV can express foreign genes.
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Registered trials
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