ArticleJournal of virology2011
Encephalomyocarditis virus 2A protein is required for viral pathogenesis and inhibition of apoptosis.
Article in Journal of virology, 2011. 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 EMCV protein 2B* is required for efficient cell lysis via both caspase-3-dependent and -independent pathways during infection.The Journal of general virology · 2025Article
- The complex interplay between encephalomyocarditis virus and the host defence system.Virulence · 2024Review
- Comprehensive Elucidation of the Role of L and 2A Security Proteins on Cell Death during EMCV Infection.Viruses · 2024Article
- Directed Evolution of Seneca Valley Virus in Tumorsphere and Monolayer Cell Cultures of a Small-Cell Lung Cancer Model.Cancers · 2023Article
- Encephalomyocarditis Virus 2A Protein Inhibited Apoptosis by Interaction with Annexin A2 through JNK/c-Jun Pathway.Viruses · 2022Article
- Insights from structural studies of the cardiovirus 2A protein.Bioscience reports · 2022Review
- MicroRNA-detargeting proves more effective thanMolecular therapy oncolytics · 2021Article
- Structural and molecular basis for Cardiovirus 2A protein as a viral gene expression switch.Nature communications · 2021Article
- Molecular characterization of encephalomyocarditis virus strains isolated from an African elephant and rats in a French zoo.Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc · 2021Article
- Egress of non-enveloped enteric RNA viruses.The Journal of general virology · 2021Review
- From pyroptosis, apoptosis and necroptosis to PANoptosis: A mechanistic compendium of programmed cell death pathways.Computational and structural biotechnology journal · 2021Review
- Regulators of Viral Frameshifting: More Than RNA Influences Translation Events.Annual review of virology · 2020Review
- Viroporins and inflammasomes: A key to understand virus-induced inflammation.The international journal of biochemistry & cell biology · 2020Review
- The location of sensing determines the pancreatic β-cell response to the viral mimetic dsRNA.The Journal of biological chemistry · 2020Article
- VPg unlinkase/TDP2 in cardiovirus infected cells: Re-localization and proteolytic cleavage.Virology · 2018Article
- Structures and Corresponding Functions of Five Types of Picornaviral 2A Proteins.Frontiers in microbiology · 2017Review
- Identification of Novel Rosavirus Species That Infects Diverse Rodent Species and Causes Multisystemic Dissemination in Mouse Model.PLoS pathogens · 2016Article
- AMP-activated protein kinase phosphorylates EMCV, TMEV and SafV leader proteins at different sites.Virology · 2014Article
- The encephalomyocarditis virus.Virulence · 2012Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The encephalomyocarditis virus (EMCV), a Picornaviridae virus, has a wide host spectrum and can cause various diseases. EMCV virulence factors, however, are as yet ill defined. Here, we demonstrate that the EMCV 2A protein is essential for the pathogenesis of EMCV. Infection of mice with the B279/95 strain of EMCV resulted in acute fatal disease, while the clone C9, derived by serial in vitro passage of the B279/95 strain, was avirulent. C9 harbored a large deletion in the gene encoding the 2A protein. This deletion was incorporated into the cDNA of a pathogenic EMCV1.26 strain. The new virus, EMCV1.26Δ2A, was capable of replicating in vitro, albeit more slowly than EMCV1.26. Only mice inoculated with EMCV1.26 triggered death within a few days. Mice infected with EMCV1.26Δ2A did not exhibit clinical signs, and histopathological analyses showed no damage in the central nervous system, unlike EMCV1.26-infected mice. In vitro, EMCV1.26Δ2A presented a defect in viral particle release correlating with prolonged cell viability. Unlike EMCV1.26, which induced cytopathic cell death, EMCV1.26Δ2A induced apoptosis via caspase 3 activation. This strongly suggests that the 2A protein is required for inhibition of apoptosis during EMCV infection. All together, our data indicate that the EMCV 2A protein is important for the virus in counteracting host defenses, since Δ2A viruses were no longer pathogenic and were unable to inhibit apoptosis in vitro.
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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.