At present, most studies on PSV conducted domestically and abroad have been epidemiological investigations, and few studies have examined pathogenicity and mechanism of this virus. In this report, we describe the isolation of a PSV strain, SHCM2019, from pig farms in Shanghai. The strain was identified as PSV by RT-PCR, IFA and TEM assays, and its pathogenicity in piglets was confirmed.
To further characterize this strain, we sequenced the complete genome of the SHCM2019 strain. The full-length genome of the strain was determined to 7,567 nucleotides, consisting of a 5' UTR of 465 nucleotides, a 3' UTR of 106 nucleotides, and a single open reading frame (ORF) of 6,996 nucleotides that encodes a protein precursor of 2,331 amino acids. BLAST results showed that the nucleotide similarity between the isolates and PSV-YC2011 was as high as 90%. The antigenic epitome analysis of VP1 showed that the SHCM2019 strain was not significantly different from other PSV strains, and the slow evolution of PSV strain could help to better control the disease.
Phylogenetic analysis based on the polyprotein gene showed that the PSV isolates from China had genetic diversity, and were closely related to the South Korean strain, but were distantly related to the PSV isolates from Europe and America, suggesting that the transmission of PSV may be significantly affected by the region. At the same time, we constructed an evolutionary tree of the VP1 gene (see additional file 1), but the topological structure and branching of the evolutionary tree were slightly different from the protein coding region, and were not completely consistent with the previously reported evolutionary tree of VP1 [24], which indicated that PSV could not be divided into genotypes at present. The VP1 protein, located in the outermost layer of PSV virions, is the main protein that enteroviruses induce the body to produce neutralizing antibodies and maintain viral infection [25]. At present, many picornaviruses are genotyped by VP1 sequence alignment [26].
The driving forces of viral evolution include gene mutation, natural selection, gene drift, and viral gene recombination. Mutation and recombination are two important mechanisms governing virus evolution. The results of recombination analysis showed that there was recombination between PSV isolates, and the recombination sites may be located in the 3D region, which was not consistent with the findings of previous studies [24, 27–29]. The 3D protein is a virus-specific RNA polymerase [3], and its ability to synthesize is, in turn, an important factor affecting recombination. In view of the diversity of recombination sites reported to date [24, 27–29], we must accelerate the process of research on the molecular mechanism of PSV.
The PSV infection rate was high in both domestic and wild pigs [9], but in most cases, the pigs infected with PSV did not exhibit clinical symptoms [8, 9, 14, 20], which suggests that PSV is not consistently pathogenic. As a result, when there is mass diarrhea in a swine herd, most researchers mainly focus on porcine circovirus type 2 (PCV-2) and porcine epidemic diarrhoea virus (PEDV), while PSV, which can cause similar symptoms, does not attract similar attention [30, 31]. In this study, the SHCM2019 strain was found to replicate in the intestinal tracts of piglets and cause diarrhoea and a degree of pneumonia in pigs, suggesting that the SHCM2019 strain is pathogenic. PCV-2 infection itself is asymptomatic, and infected pigs occasionally develop severe postweaning multisystem depletion syndrome under viral coinfection or immune stimulation [32]. Similarly, PSV may also require currently unidentified factors to show full pathogenicity in pigs, which warrant further investigation.