ArticleMedical microbiology and immunology2004
Characterization of coxsackievirus B3-caused apoptosis under in vitro conditions.
Article in Medical microbiology and immunology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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Who cites it
8 citing papers in PubMed, 25 citations in OpenAlex.
- Novel Insights into the Kallikrein-Kinin System in Fulminant Myocarditis: Physiological Basis and Potential Therapeutic Advances.Journal of inflammation research · 2024Review
- The protection effects of survivin in the cell model of CVB3-induced viral myocarditis.Heart and vessels · 2020Article
- Regulation of Apoptosis by Enteroviruses.Frontiers in microbiology · 2020Review
- Engineering Enhanced Vaccine Cell Lines To Eradicate Vaccine-Preventable Diseases: the Polio End Game.Journal of virology · 2016Article
- The anti-obesity drug orlistat reveals anti-viral activity.Medical microbiology and immunology · 2015Article
- Characterization of coxsackievirus B3 replication in human umbilical vein endothelial cells.Medical microbiology and immunology · 2014Article
- Coxsackievirus B3-induced cellular protrusions: structural characteristics and functional competence.Journal of virology · 2011Article
- Stress-activated protein kinases are involved in coxsackievirus B3 viral progeny release.Journal of virology · 2005Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Among several mechanisms of pathogenesis of the frequent and sometimes serious infections with coxsackievirus B3 (CVB3), one detail is apoptosis. Recently, a new apoptotic mechanism involving the specific interaction between the capsid protein VP2 of the highly virulent variant CVB3H3 and the proapoptotic host protein Siva was identified. The relevance of this observation for virus pathogenicity was shown in a BALB/c mouse model using CVB3H3 and the interaction-deficient mutant virus CVB3H310A1. In this study these results were verified and extended under in vitro conditions. The different apoptotic capability of CVB3H3 versus CVB3H310A1 was demonstrated by apoptotic nuclear condensation, DNA fragmentation, expression of Siva mRNA, and caspase-3 activation. The virus-specific differences were caused by the VP2 capsid proteins, which was shown by overexpression of the single VP2H3 and VP2H310A1 protein. Furthermore, the involvement of apoptosis in virus progeny production and the associated appearance of the cytopathic effect was demonstrated by application of the pan-caspase inhibitor Z-VAD-FMK. These in vitro results indicate that the induction of apoptosis during CVB3H3 infection is based on the interaction between the capsid protein VP2 and the proapoptotic protein Siva, independently from the complex situation in vivo.
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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.