4.6 Article

Proteogenomics Uncovers Critical Elements of Host Response in Bovine Soft Palate Epithelial Cells Following In Vitro Infection with Foot-And-Mouth Disease Virus

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VIRUSES-BASEL
卷 11, 期 1, 页码 -

出版社

MDPI
DOI: 10.3390/v11010053

关键词

foot-and-mouth disease virus (FMDV); bovine soft palate; nasopharynx; transcriptomics; proteomics; bioinformatics; virus-host interaction; innate immune system; interferon-stimulated genes (ISG)

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资金

  1. Swedish Research Council (Formas, Sweden)
  2. L'Agence Nationale de la Recherche (ANR, France)
  3. Federal Office for Agriculture and Food (BLE, Germany) through the ANIHWA ERA-Net project TRANSCRIPTOVAC

向作者/读者索取更多资源

Foot-and-mouth disease (FMD) is the most devastating disease of cloven-hoofed livestock, with a crippling economic burden in endemic areas and immense costs associated with outbreaks in free countries. Foot-and-mouth disease virus (FMDV), a picornavirus, will spread rapidly in naive populations, reaching morbidity rates of up to 100% in cattle. Even after recovery, over 50% of cattle remain subclinically infected and infectious virus can be recovered from the nasopharynx. The pathogen and host factors that contribute to FMDV persistence are currently not understood. Using for the first time primary bovine soft palate multilayers in combination with proteogenomics, we analyzed the transcriptional responses during acute and persistent FMDV infection. During the acute phase viral RNA and protein was detectable in large quantities and in response hundreds of interferon-stimulated genes (ISG) were overexpressed, mediating antiviral activity and apoptosis. Although the number of pro-apoptotic ISGs and the extent of their regulation decreased during persistence, some ISGs with antiviral activity were still highly expressed at that stage. This indicates a long-lasting but ultimately ineffective stimulation of ISGs during FMDV persistence. Furthermore, downregulation of relevant genes suggests an interference with the extracellular matrix that may contribute to the skewed virus-host equilibrium in soft palate epithelial cells.

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