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

• Published in: Virus research Vol. 339; p. 199282
• Main Authors: Burgher-Pulgaron, Yaima, Provost, Chantale, Alvarez, Fernando, Meza-Serrano, Europa, Pesant, Marie-Jeanne, Price, Christopher A., Gagnon, Carl A.
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 02.01.2024; Elsevier
• Subjects: Animals; Circovirus - genetics; Co-infection; Coinfection; DUSP1; NPTr-CD163 cells; PCV2b; Porcine Reproductive and Respiratory Syndrome; Porcine respiratory and reproductive syndrome virus; PRRSV; Swine; Swine Diseases; Virus Replication; Co-infection; PCV2b; DUSP1; NPTr-CD163 cells; PRRSV
• ISSN: 0168-1702; 1872-7492
• DOI: 10.1016/j.virusres.2023.199282

•NPTr-CD163 cells can be used as a model of swine epithelial respiratory cells for PCV2b/PRRSV co-infection studies.•PCV2b and PRRSV co-infection enhances PCV2b replication and decreases PRRSV replication in NPTr-CD163 cells.•PCV2b and PRRSV co-infection alters cytokine mRNA expression and modulates the expression of cellular genes and biological processes.•PCV2b and PRRSV infections upregulates DUSP1 expression.•Transient knockdown of DUSP1 reduces PCV2b replication while it enhances PRRSV replication in co-infected cells. 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.