Discussion
HP-PRRSV infection induces higher rates of morbidity and mortality in animals of different ages than PRRSV infection[
5,
6,
21,
22]. However, differences in the lesions on peripheral immune organs and lungs following experimental infection of pigs with highly pathogenic and classical PRRSV have not yet to be reported. In this study, higher viral loads were detected in peripheral immune organs (tonsils, ILNs, spleens) and lungs of piglets infected with the HP-PRRSV HuN4 strain than that of pigs infected with the classical PRRSV CH-1a strain. Viral replication in these organs leads to the serious lesions (Table
1). Depletion of peripheral immune organs adversely affects the capacity for eradication of viruses and bacteria, and immunity to endogenous and exogenous substances with a variety of specific morphological and functional consequences. HuN4 infection causes severe immunosuppression and enhances susceptibility to secondary infections and also induces severe thymic atrophy[
13]. The severe damage to immune organs and lungs mediated by HuN4 may cause the high mortality rate associated with HP-PRRS in pigs.
Besides the apoptosis observed in thymocytes[
13], significant numbers of apoptotic cells were also observed in tonsils, ILNs, spleen and lungs of piglets infected with HuN4 (Table
2). However, few apoptotic cells were detected in these tissues of piglets infected with CH-1a, which was consistent with the results of previous studies of cell apoptosis induced by classical PRRSV infection[
10,
23,
24]. Large numbers of apoptotic cells in these organs induced by HuN4 infection indicated that apoptosis may play a role in the pathogenesis of the HP-PRRS, with increased apoptotic cells associated both with more severe tissue injury and with increased viral loads. Moreover, more apoptotic cells were observed in immune organs of HP-PRRSV infected piglets pointing out a mechanism which might play a role in the induction of the erratic host immune response observed in HP-PRRSV infected pigs[
14]. The apoptotic cells, along with the subsequent microscopical and gross lesions may trigger events that immune balance and induce immunosuppression. However, a specific association between cell apoptosis and PRRSV infection requires further investigation.
In conclusion, this is the first report describing a comparative investigation of apoptotic cells in peripheral immune organs and lungs of piglets following experimental infection with the highly pathogenic and classical PRRSV strains. Large numbers of apoptotic cells in immune organs and lung induced by HuN4 infection may play a role in the pathogenesis of the HP-PRRS.
Acknowledgements
This work was supported by grants from the National Natural Science Foundation for Young Scholars of China (31201885), the Science and Technology Research Project of Harbin (2010AA6AN083) and the Fundamental Research Funds of Chinese Academy of Agricultural Sciences (2012ZL079/SKLVBP201317-5).
Competing interests
The authors declare that they have no competing interests.
Authors’ contributions
Conceived and designed the experiments: CXH and WG; Performed the experiments: WG, HYL, LYG, HZF, JCG, WSJ and SWD. Critical discussion and final approval of manuscript: WG, HYL, TYB, LYG, ZEM, HZF, JCG, WSJ, SWD, CXH. All authors approved the final manuscript.