ArticleFrontiers in veterinary science2020
Mechanisms of Maintenance of Foot-and-Mouth Disease Virus Persistence Inferred From Genes Differentially Expressed in Nasopharyngeal Epithelia of Virus Carriers and Non-carriers.
Article in Frontiers in veterinary science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- The whole genome sequencing offers insights into the susceptibility to the foot-and-mouth disease virus carrier state.Veterinary research · 2026Article
- Article
- The pathogenesis of foot-and-mouth disease virus: current understandings and knowledge gaps.Veterinary research · 2025Review
- Use of virus-like particles and nanoparticle-based vaccines for combating picornavirus infections.Veterinary research · 2024Review
- The genetic architecture of complete blood counts in lactating Holstein dairy cows.Frontiers in genetics · 2024Article
- Inferred Causal Mechanisms of Persistent FMDV Infection in Cattle from Differential Gene Expression in the Nasopharyngeal Mucosa.Pathogens (Basel, Switzerland) · 2022Article
- Screening the hub genes and analyzing the mechanisms in discharged COVID-19 patients retesting positive through bioinformatics analysis.Journal of clinical laboratory analysis · 2022Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Foot-and-mouth disease virus (FMDV) causes persistent infection of nasopharyngeal epithelial cells in ~50% of infected ruminants. The mechanisms involved are not clear. This study provides a continued investigation of differentially expressed genes (DEG) identified in a previously published transcriptomic study analyzing micro-dissected epithelial samples from FMDV carriers and non-carriers. Pathway analysis of DEG indicated that immune cell trafficking, cell death and hematological system could be affected by the differential gene expression. Further examination of the DEG identified five downregulated (chemerin, CCL23, CXCL15, CXCL16, and CXCL17) and one upregulated (CCL2) chemokines in carriers compared to non-carriers. The differential expression could reduce the recruitment of neutrophils, antigen-experienced T cells and dendritic cells and increase the migration of macrophages and NK cells to the epithelia in carriers, which was supported by DEG expressed in these immune cells. Downregulated chemokine expression could be mainly due to the inhibition of canonical NFκB signaling based on DEG in the signaling pathways and transcription factor binding sites predicted from the proximal promoters. Additionally, upregulated CD69, IL33, and NID1 and downregulated CASP3, IL17RA, NCR3LG1, TP53BP1, TRAF3, and TRAF6 in carriers could inhibit the Th17 response, NK cell cytotoxicity and apoptosis. Based on our findings, we hypothesize that (1) under-expression of chemokines that recruit neutrophils, antigen-experienced T cells and dendritic cells, (2) blocking NK cell binding to target cells and (3) suppression of apoptosis induced by death receptor signaling, viral RNA, and cell-mediated cytotoxicity in the epithelia compromised virus clearance and allowed FMDV to persist. These hypothesized mechanisms provide novel information for further investigation of persistent FMDV infection.
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