DUSP1 mRNA modulation during porcine circovirus type 2 and porcine reproductive and respiratory syndrome virus co-infection regulates viruses replication
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11 décembre 2023
- handle: 10670/1.1reb5j
- doi: 10.1016/j.virusres.2023.199282
CC BY-NC 4.0 DEED Attribution - Pas d’Utilisation Commerciale 4.0 International , https://creativecommons.org/licenses/by-nc/4.0/deed.fr
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PCV2b PRRSV Co-infection NPTr-CD163 cells DUSP1Sujets proches
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Yaima Burgher Pulgaron et al., « DUSP1 mRNA modulation during porcine circovirus type 2 and porcine reproductive and respiratory syndrome virus co-infection regulates viruses replication », Papyrus : le dépôt institutionnel de l'Université de Montréal, ID : 10.1016/j.virusres.2023.199282
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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.