ArticlePloS one2011
Equine torovirus (BEV) induces caspase-mediated apoptosis in infected cells.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Serpentoviruses Exhibit Diverse Organization and ORF Composition with Evidence of Recombination.Viruses · 2024Article
- Activation of the autophagy pathway by Torovirus infection is irrelevant for virus replication.PloS one · 2019Article
- Transcriptional and Translational Landscape of Equine Torovirus.Journal of virology · 2018Article
- Nidovirus-Associated Proliferative Pneumonia in the Green Tree Python (Morelia viridis).Journal of virology · 2017Article
- Ultrastructural characterization of membranous torovirus replication factories.Cellular microbiology · 2016Article
- RNA disruption is associated with response to multiple classes of chemotherapy drugs in tumor cell lines.BMC cancer · 2016Article
- Molecular epidemiology of Porcine torovirus (PToV) in Sichuan Province, China: 2011-2013.Virology journal · 2014Article
- Evolution and homologous recombination of the hemagglutinin-esterase gene sequences from porcine torovirus.Virus genes · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toroviruses are gastroenteritis causing agents that infect different animal species and humans. To date, very little is known about how toroviruses cause disease. Here, we describe for the first time that the prototype member of this genus, the equine torovirus Berne virus (BEV), induces apoptosis in infected cells at late times postinfection. Observation of BEV infected cells by electron microscopy revealed that by 24 hours postinfection some cells exhibited morphological characteristics of apoptotic cells. Based on this finding, we analyzed several apoptotic markers, and observed protein synthesis inhibition, rRNA and DNA degradation, nuclear fragmentation, caspase-mediated cleavage of PARP and eIF4GI, and PKR and eIF2α phosphorylation, all these processes taking place after peak virus production. We also determined that both cell death receptor and mitochondrial pathways are involved in the apoptosis process induced by BEV. BEV-induced apoptosis at late times postinfection, once viral progeny are produced, could facilitate viral dissemination in vivo and contribute to viral pathogenesis.
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