DUSP1 mRNA modulation during porcine circovirus type 2 and porcine reproductive and respiratory syndrome virus co-infection regulates viruses replication


Article
Version publiée / Version of Record

Date de publication

Identifiant ORCID de l’auteur

Contributrices et contributeurs

Direction de recherche

Publié dans

Virus research

Date de la Conférence

Lieu de la Conférence

Éditeur

Elsevier

Cycle d'études

Programme

Mots-clés

  • PCV2b
  • PRRSV
  • Co-infection
  • NPTr-CD163 cells
  • DUSP1

Organisme subventionnaire

Résumé

Résumé

The effects of porcine circovirus type 2b (PCV2b) and porcine reproductive and respiratory syndrome virus (PRRSV) co-infection in epithelial cells of the swine respiratory tract is unknown. In the present study, the newborn pig trachea cell line NPTr-CD163, which is permissive to both viruses, was persistently infected with PCV2b and then with PRRSV. Viral replication, cell viability, cytokines’ mRNA expression, and modulation of cellular genes expression were evaluated in infected cells. In NPTr-CD163 co-infection model, PCV2b replication was enhanced while PRRSV replication was suppressed. Cell viability was significantly decreased during PCV2b single infection and co-infection compared to mock-infected and PRRSV single infected cells. However, no difference was observed in cell viability between PCV2b and PCV2b/PRRSV infected cells. The IL6, IL8 and IL10 mRNA expression was significantly higher in co-infected cells compared to PCV2b and PRRSV single infected cells. Moreover, the IFN-α/β expression was significantly reduced in co-infected cells compared to PCV2b infected cells whereas it remained higher compared to PRRSV infected cells. The differential gene expression analysis revealed that the mRNA expression level of the cellular gene DUSP1 was significantly higher in all PRRSV infection models compared to PCV2b single infected cells. Knockdown of DUSP1 expression in co-infected cells significantly reduced PCV2b replication, suggesting a role for DUSP1 in PCV2b/PRRSV pathogenesis.

Table des matières

Notes

Notes

Autre version linguistique

Ensemble de données lié

Licence

CC BY-NC 4.0 DEED Attribution - Pas d’Utilisation Commerciale 4.0 International

Approbation

Évaluation

Complété par

Référencé par

Ce document diffusé sur Papyrus est la propriété exclusive des titulaires des droits d'auteur et est protégé par la Loi sur le droit d'auteur (L.R.C. (1985), ch. C-42). Sauf si le document est diffusé sous une licence Creative Commons, il ne peut être utilisé que dans le cadre d'une utilisation équitable et non commerciale comme le prévoit la Loi (i.e. à des fins d'étude privée ou de recherche, de critique ou de compte-rendu). Pour toute autre utilisation, une autorisation écrite des titulaires des droits d'auteur sera nécessaire.