Abstract
Canine parvovirus type 2 (CPV-2) and feline panleukopenia virus (FPV) cause severe disease in young animals, pups, and kittens. CPV-2 evolved from FPV by altering the species-specific binding of the viral capsid to the host receptor, i.e., the transferrin receptor (TfR), and CPV-2 genetic variants have been identified by specific VP2 amino acid residues (297, 426). Early studies focused on the main capsid protein VP2; however, there have been limited studies on the non-structural protein NS1. In this study, we identified the genetic variants of clinical samples in dogs and cats in northern China during 2019-2020. The genetic characterization and phylogenetic analyses of VP2 and NS1 gene were also conducted. The results revealed that the CPV-2c was identified as the major genetic variant. One new CPV-2b and two CPV-2c strains were collected from cats. Four mutation sites (60, 630, 443, and 545 amino acid residues) were located in the functional domains of the NS1 protein. The phylogenetic analysis of VP2 and NS1 genes showed that they were clustered by geographical regions and genotypes. The gene mutation rate of CPV-2 was increasing in recent years, resulting in a complex pattern of gene evolution in terms of host preference, geographical selection, and new genetic variants. This study emphasizes that continuous molecular epidemiological surveillance is required to understand the genetic diversity of FPV and CPV-2 strains.