ArticleProteomics. Clinical applications2018
Understanding TGEV-ETEC Coinfection through the Lens of Proteomics: A Tale of Porcine Diarrhea.
Article in Proteomics. Clinical applications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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
6 citing papers in PubMed.
- Development of a High-Resolution Melting (HRM)-Based Multiplex Real-Time PCR Assay of PEDV, TGEV, PoRV, PDCoV, PRV, and PRRSV.Transboundary and emerging diseases · 2026Article
- Persistence Infection of TGEV PromotesInternational journal of molecular sciences · 2022Article
- Bacterial and Viral Co-Infection in the Intestine: Competition Scenario and Their Effect on Host Immunity.International journal of molecular sciences · 2022Review
- EIF4A2 interacts with the membrane protein of transmissible gastroenteritis coronavirus and plays a role in virus replication.Research in veterinary science · 2019Article
- Understanding TGEV-ETEC Coinfection through the Lens of Proteomics: A Tale of Porcine Diarrhea.Proteomics. Clinical applications · 2018Article
- Porcine transmissible gastroenteritis virus nonstructural protein 2 contributes to inflammation via NF-κB activation.Virulence · 2018Article
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2 authors.
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Abstract
Porcine diarrhea and gastroenteritis are major causes of piglet mortality that result in devastating economic losses to the industry. A plethora of pathogens can cause these diseases, with the transmissible gastroenteritis virus (TGEV) and enterotoxigenic Escherichia coli K88 (ETEC) being two of the most salient. In the December 2017 issue of Proteomics Clinical Aplications, Xia and colleagues used comparative proteomics to shed light on how these microbes interact to cause severe disease . The authors discovered that TGEV induces an epithelial-mesenchymal transition-like phenotype that augments cell adhesion proteins mediating the attachment of ETEC to intestinal epithelial cells. Moreover, coinfection was found to modulate several host proteins that could bolster pathogen persistence. Importantly, the authors observed that ETEC suppresses the production of inflammatory cytokines induced by TGEV, which may in turn promote the long-term survival of both microbes.
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