2.3 Swine Influenza Virus

Swine influenza virus (SwIV), which belongs to Orthomyxoviridaefamily, causes seasonal epidemic or occasional pandemic outbreaks in pigs worldwide (Taubenberger & Morens, 2008). SwIV can be subdivided into many subtypes, including influenza A, B, and C (Baudon, Peyre, Peiris, & Cowling, 2017; Meiners et al., 2014).
PRDC is an economically enormous problem accompanied by slow growth performance, cough, poor food utilization etc(Baudon et al., 2017). It has been reported that SwIV and Mhp play important roles in PRDC (Deblanc et al., 2016; Deblanc et al., 2012; Fablet, Marois-Crehan, et al., 2012). SwIV can target and replicate in epithelial cells of the upper respiratory tract (Brown, Alexander, Chakraverty, Harris, & Manvell, 1994). Coinfection with SwIV and Mhp was detected in 23 (31%) cases in 74 lungs from 2009 to 2015 retrospective analysis (Rech et al., 2018). Although the interaction between SwIV and Mhp is minimal or even appear independent of each other (Thacker, Thacker, & Janke, 2001), the pre-infection with Mhp was remarkably exacerbated by the clinical symptoms of pigs with H1N1 infection during the first week after virus inoculation (Deblanc et al., 2016). Furthermore, the pig lung lesion caused by inoculation with Mhp and SwIV was more severe than those inoculated with Mhp only (Yazawa et al., 2004). Deblanc and co-workers indicated that clinical signs and macroscopic lung lesions were similar in early time post-H1N1 inoculation compared to pre-Mhp infection or not pig group, and Mhp didn’t affect the influenza virus replication and the IFN-induced antiviral responses in the lung, however, there is a higher inflammatory response to H1N1 infection in pre-Mhp infection group. The exact mechanism can be revealed by the massive infiltration of neutrophils and macrophages into the lungs and the increased production of pro-inflammatory cytokines (IL-6, IL-1β and TNF-α) (Deblanc et al., 2016). Moreover, Deblanc demonstrated that Mhp and H1N1 appeared to act synergistically, as Mhp and H1N2 would compete in pigs that were previously infected with Mhp, resulting in the elimination of Mhp in the lung diaphragmatic lobes by the H1N2 (Deblanc et al., 2012). Furthermore, the miRNAs were differentially expressed (DE) and most of them were downregulated to defend the H1N1 in pulmonary alveolar macrophages during the process of H1N1 infection (Jiang et al., 2015). According to the different level of oxidative stress induced by pre-infection of Mhp, there were different outcomes from the subsequent infection with H1N1 subtype (Deblanc et al., 2013).
These results demonstrated that SwIV did not affect Mhp replication in the co-infected pig, but both Mhp and SwIV decreased or disrupt the function of the mucociliary apparatus and immunosuppression which potentially led to an increased secondary infections from opportunistic organisms under field conditions(DeBey & Ross, 1994).