Porcine Circovirus Modulates Swine Influenza Virus Replication in Pig Tracheal Epithelial Cells and Porcine Alveolar Macrophages

Viruses. 2023 May 20;15(5):1207. doi: 10.3390/v15051207.

Abstract

The pathogenesis of porcine circovirus type 2b (PCV2b) and swine influenza A virus (SwIV) during co-infection in swine respiratory cells is poorly understood. To elucidate the impact of PCV2b/SwIV co-infection, newborn porcine tracheal epithelial cells (NPTr) and immortalized porcine alveolar macrophages (iPAM 3D4/21) were co-infected with PCV2b and SwIV (H1N1 or H3N2 genotype). Viral replication, cell viability and cytokine mRNA expression were determined and compared between single-infected and co-infected cells. Finally, 3'mRNA sequencing was performed to identify the modulation of gene expression and cellular pathways in co-infected cells. It was found that PCV2b significantly decreased or improved SwIV replication in co-infected NPTr and iPAM 3D4/21 cells, respectively, compared to single-infected cells. Interestingly, PCV2b/SwIV co-infection synergistically up-regulated IFN expression in NPTr cells, whereas in iPAM 3D4/21 cells, PCV2b impaired the SwIV IFN induced response, both correlating with SwIV replication modulation. RNA-sequencing analyses revealed that the modulation of gene expression and enriched cellular pathways during PCV2b/SwIV H1N1 co-infection is regulated in a cell-type-dependent manner. This study revealed different outcomes of PCV2b/SwIV co-infection in porcine epithelial cells and macrophages and provides new insights on porcine viral co-infections pathogenesis.

Keywords: co-infection; epithelial cells; macrophages; porcine circovirus; swine influenza A virus; viral pathogenesis; virus replication.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Circoviridae Infections* / veterinary
  • Circovirus* / genetics
  • Coinfection*
  • Epithelial Cells
  • Influenza A Virus, H1N1 Subtype* / genetics
  • Influenza A Virus, H3N2 Subtype / genetics
  • Macrophages, Alveolar
  • Orthomyxoviridae Infections*
  • RNA, Messenger
  • Swine
  • Swine Diseases*
  • Virus Replication

Substances

  • RNA, Messenger

Grants and funding

This project was funded by a Natural Sciences and Engineering Research Council of Canada (NSERC) discovery grant (number RGPIN-2017-05240). C.A. Gagnon is financially supported by a Canadian Swine Research and Development Cluster (CSRDC) research project, Les Éleveurs de porcs du Québec and by Probiotech International (number 1781). Y. Burgher was a recipient of a graduate student scholarship from the Fonds de recherche du Québec–Nature et technologie (FRQNT). Y. Burgher and M.J. Pesant were also recipients of graduate student scholarships from the Swine and poultry infectious diseases research center (Centre de recherche en infectiologie porcine et avicole, CRIPA-FRQ) and of different graduate student merit scholarships for Graduate and Postdoctoral Studies from the Université de Montréal.