ArticleBMC veterinary research2018
Transcriptomic analysis reveals that enterovirus F strain SWUN-AB001 infection activates JNK/SAPK and p38 MAPK signaling pathways in MDBK cells.
Article in BMC veterinary research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Differentially Expressed miRNA Profiles in Serum-Derived Exosomes from Cattle Infected with Lumpy Skin Disease Virus.Pathogens (Basel, Switzerland) · 2025Article
- GRP78 recognizes EV-F 3D protein and activates NF-κB to repress virus replication by interacting with CHUK/IKBKB.Journal of virology · 2024Article
- Multiple Types of Novel Enteric Bopiviruses (Viruses · 2021Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
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Abstract
backgroundEnteroviruses (Picornaviridae family) have been widely detected in the feces from cattle with diarrhea. However, the mechanisms responsible for the pathogenicity of enteroviruses in cattle remain unclear. Recently, we isolated a novel EV-F7 strain called SWUN-AB001 from diarrheal yak (Bos grunniens) feces. To explore the pathogenic mechanisms of this novel virus, we used a transcriptomics approach to find genes with differential expression patterns in Madin-Darby bovine kidney (MDBK) cells during infection with SWUN-AB001 over time.
resultsMDBK cells were sampled at 12 and 24 h post-infection (hpi) to represent the early and late stages of a SWUN-AB001 infection. Compared with the non-infected cells, 19 and 1050 differentially expressed genes (DEGs) were identified at 12 and 24 hpi, respectively. These DEGs were associated with disease, signal transduction, cellular process and cytokine signaling categories. At 24 hpi, the pathway enrichment analysis revealed that signal pathways such as c-Jun NH2-terminal kinase/ stress-activated protein kinase (JNK/SAPK) and mitogen-activated protein kinase (MAPK) pathways and cytokine-cytokine receptor interactions were associated with the interactions occurring between EV-F7 and MDBK cells. Our additional western blot analysis showed that the phosphorylation levels of JNK/SAPK and p38 MAPK proteins increased significantly in the MDBK cells at 24 hpi. The result indicated that infection with EV-F7 could activate JNK/SAPK and p38 MAPK pathways in MDBK cells, and possibly trigger large-scale cytokine production.
conclusionOur transcriptome analysis provides useful initial data towards better understanding of the infection mechanisms used by EV-F7, while highlighting the potential molecular relationships occurring between the virus and the host's cellular components.
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