PSV is widely popular among pig population in China. In this study, a PSV isolate from pig farms in Shanghai, SHCM2019, was identified and sequenced. The isolated strain has 7,567 nucleotides, consisting of a 5' UTR of 465 nucleotides, a 3' UTR of 106 nucleotides, and a single ORF of 6,996 nucleotides that encodes a polyprotein precursor of 2,331 amino acids. The lengh of the 5' UTR is varied in PSVs. According to previous research, the 5′ terminal residues of the complete picornavirus should be UU [5], but the two 5′ terminal residues were AC for strain SHCM2019, which was not accordance with those sequence features. The antigenic epitome of VP1 had high identity with other PSV strains, indicating the slow evolution, which will provide useful clues for disease prevention.
Phylogenetic analysis based on the polyprotein gene revealed that the PSV isolates from China exhibit genetic diversity, and are closely related to the South Korean strains, but are distantly related to the PSV isolates from Europe and America, suggesting that the prevalence of PSVs may has certain territoriality. Furthermore, we constructed an evolutionary tree of the VP1 gene (Supplementary Fig. 2). However, the topological structure and phylogenetic branching of the VP1 tree were slightly different from the ORF tree and the VP1 tree previously reported [23], which indicated that PSV could not be divided into genotypes at present. At present, many picornaviruses are genotyped by VP1 sequence alignment[24]. The classification criterion is that the VP1 sequence difference between isolates is greater than 25% [25]. Among PSVs, the nucleotide and amino acid sequence identities of the VP1 region were > 70.8% and > 75.1%, respectively, and these values were less multiple than those of porcine enteroviruses (> 53.9% and > 53.3%, respectively) [24]. This might be one of the reasons why the genotyping PSVs is considered to be hard.
The driving forces of viral evolution include gene mutation, natural selection, gene drift, and viral gene recombination. In which, mutation and recombination are two important mechanisms. The results of recombination analysis showed recombination existed among the PSV isolates, however, the recombination site was located in the 3D region, which was not consistent with the previous studies [23, 26–28]. The 3D protein is a virus-specific RNA polymerase[3], which has the ability to synthesize viral RNA, and its recombination plays an important role in viral replication. In view of the diversity of recombination sites reported to date [23, 26–28], we must accelerate the process of research on the molecular mechanism of PSV.
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. In clinic, like porcine circovirus type 2 (PCV2), 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. This also led to PCV2 and PEDV being the main focus of most researchers when large-scale diarrhea occurred in pig populations, while, PSV, which could cause similar symptoms, didn't attract similar attention [29, 30]. Perhaps PSV require currently unidentified factors to show full pathogenicity in pigs, which warrant further investigation.