The complete genome sequence of Seneca Valley virus (SVV), a single-stranded RNA virus that causes porcine vesicular disease in China, has been sequenced and analyzed. This Chinese isolate shares 94.4 to 97.1% sequence identity to another 8 strains from Canada, Brazil, and the United States. This is the first report of SVV infecting swine in China.

Summary The pathogenesis of highly pathogenic porcine reproductive and respiratory syndrome virus (PRRSV) strain (HuN4) is poorly understood. Therefore, highly pathogenic PRRSV strain (HuN4) and its derivative strain (HuN4‐F112) (obtained by propagation in MARC145 cells for 112 passages) were inoculated into a total of 48 PRRSV‐sero‐negative pigs (age: 4–5 weeks) by the intranasal route. Virological, pathological and in situ hybridization analyses were performed. The results exhibited that pigs infected with HuN4 showed a loss of appetite, decrease in body weight, raised body temperature and respiratory symptoms, along with interstitial pneumonia lesions. In the HuN4 group, multifocal interstitial pneumonia with macrophage infiltration was found in the lung. The lesions in the lymph node were characterized by collapsed follicles, depletion of germinal centres and reduction in lymphocytes. Perivascular cuffing and glial nodules were observed in the brains of some pigs. By comparison, the HuN4‐F112 group had milder lesions. PRRSV was detected in macrophages, alveolar epithelial cells and vascular endothelial cells in the tonsil and lymph nodes. The PRRSV amounts in the pigs infected with HuN4 were 105–109 copies/ml in the blood and 1010–1011 copies/g in the lung tissues, whereas the virus amounts with HuN4‐F112 were 102.15–103.13 copies/ml in the blood and 103.0–103.6 copies/g in the lung. Our results demonstrate that the PRRS HuN4 virus infects alveolar epithelial cells, macrophages and vascular endothelial cells causing diffuse alveolar damage and lymph node necrosis. Its higher pathogenicity compared with HuN4‐F112 virus may be explained in part by higher replication rate in the previously mentioned organs.

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Inactivated virus vaccines with whole antigen spectra and good safety are the commonly used modality for preventing infections. However, the poor immunogenicity greatly limits its clinical applications. Herein, by taking advantages of the crucial roles of Se in the functions of immune cells and its biomineralization property, it successfully in‐situ synthesized Se nanoadjuvant on inactivated viruses such as porcine epidemic diarrhea virus (PEDV), pseudorabies virus (PRV), and porcine reproductive and respiratory syndrome virus (PRRSV) in a facile method, which is universal to construct other inactivated virus vaccines. The nanovaccine can highly effectively enhance the uptake of PEDV/PRV/PRRSV into dendritic cells (DCs) and activate DCs via triggering TLR4 signaling pathways and regulating selenoproteins expressions. Furthermore, it exhibited better activities in triggering macrophages and natural killer cells‐mediated innate immunity and T cells‐mediated cellular immunity compared to PEDV and the commercial inactivated PEDV vaccine on both mice and swine models. This study provides a universal Se nanoadjuvant for developing inactivated viruses‐based nanovaccines for preventing virus infections.