1 | INTRODUCTION
Canine parvovirus causes severe and fatal epidemic diseases of
hemorrhagic gastroenteritis and subacute myocarditis in dogs, cats, and
several wild carnivore species around the world (Miranda & Thompson,
2016). As a member of the Genus Protoparvovirus Parvovirinae subfamily
in the Parvoviridae family, parvovirus is a small (diameter of 25 nm),
nonenveloped virus (Cotmore et al., 2019). It has a linear,
single-stranded, negative-sense DNA genome, which consists of
approximately 5200 nucleotides (nt), including two large gene cassettes.
One of them encodes two structural (VP1 and VP2) proteins and the other
encodes two nonstructural (NS1 and NS2) proteins by alternative splicing
of the same mRNAs (Reed, Jones, & Miller, 1988). VP1 contains the
full-length VP2 sequence. However, the most abundant structural protein,
VP2, accounts for 90% of the viral capsid, representing the major
determinant of host range and virus-host interactions, and it is cleaved
to VP3 by host proteases (Decaro & Buonavoglia, 2012).
It has been estimated that this virus has a significantly higher
nucleotide substitution rate with values of approximately
10-4 substitutions/site/year, considering the genes of
VP2, NS1 and the full-length genome (Hoelzer, Shackelton, Parrish, &
Holmes, 2008). The frequent variation and evolution of CPV changes its
host range and forms virus strains with different geographical
characteristics. Amino acid substitutions in the VP2 gene have been
responsible for changes in its genetic and antigenic properties.
CPV was first reported in the late 1970s as the original type 2 (CPV-2)
and rapidly spread worldwide (Appel, Scott, & Carmichael, 1979). Within
a few years of its emergence in dogs, five amino acid mutation in VP2
(Met87Leu, Ile101Thr, Ala300Gly, Asp305Tyr, and Val555Ile) occurred,
resulting
in a distinct antigenic type CPV-2a, and it completely replaced CPV-2 as
the main epidemic strain in the world in 1980 (Shackelton, Parrish,
Truyen, & Holmes, 2005; Stucker et al., 2012). Another early variant
CPV-2b appeared in 1984, which has the Asn426Asp substitution in VP2
compared with CPV-2a (Parrish et al., 1991; Pratelli et al., 2001). In
1990, the Ser297Ala mutation appeared in VP2 of CPV-2a and CPV-2b, which
were designated as new CPV-2a and new CPV-2b accordingly (Ohshima et
al., 2008). In 2000, another antigenic variant having an amino acid
substitution (Asp426Glu), named CPV-2c, was first reported in Italy
(Buonavoglia et al., 2001), and then distributed to many parts of the
world rapidly, even becoming the predominant variant in some European
and American countries (Calderón et al., 2011; H. Wang et al., 2016).
Currently, new CPV-2a and new CPV-2b appear to have replaced the
prototype CPV-2a and CPV-2b in many countries (Zhuang et al., 2019).
In China, recent epidemiological surveys showed that the new CPV-2a and
new CPV-2b strains have been in cocirculation. Although the CPV-2c
strain has also been increasingly found since it was first discovered in
2010, the new CPV-2a and new CPV-2b strains are still the prominent CPV
genotypes in many parts of China (H. Wang et al., 2016; Wu, Li, Wang,
Liu, & Tian, 2018; Zhao et al., 2017). To further understand the
prevalence and genetic evolution of CPV-2 in Jilin province, 44 positive
samples were collected from animal hospitals in Changchun and Liaoyuan.
The VP2 genes were amplified and analyzed to determine whether the
epidemic CPV genotype has changed to provide a scientific basis for
epidemic surveillance, control and vaccine research of CPV-2.