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).