1. Introduction
In the late 1970s, canine parvovirus (CPV) emerged as a highly
contagious virus that causes severe hemorrhagic enteritis in dogs
(Carman & Povey, 1985; Kelly, 1978). The CPV origin was designated as
CPV type 2 (CPV-2) to distinguish it from canine minute virus or CPV
type 1. It is well-established that the emergence of CPV-2 resulted from
the site-specific mutation of feline panleukopenia virus or FPV-like
virus to gain the ability for replication in canine cells (Chang, Sgro,
& Parrish, 1992; Truyen & Parrish, 1992). This evidence indicates the
role of cross-species transmission. Thus, the emergence of CPV-2
variants has gained wide attention for studying its structure,
phylogenomic, and evolutionary dynamics for disease quarantine,
monitoring, and prevention.
The CPV-2 is a small, non-enveloped, single-stranded DNA virus with two
main open reading frames (ORFs). The first ORF encodes two nonstructural
proteins (NS1 and NS2) that are responsible for viral replication,
pathogenicity, and cytotoxicity. The second ORF encodes two structural
proteins (VP1 and VP2), which are related to the viral tropism and
antigenicity (Parker & Parrish, 1997; Reed, Jones, & Miller, 1988; D.
Wang, Yuan, Davis, & Parrish, 1998). Among the two structural proteins,
VP1 has the most abundant composition in the capsid, while changes in
the amino acid sequences of VP2 may alter the antigenic properties of
the virus. Thus, most studies have focused on the description of
nucleotide mutations in the VP2 gene, while information on the
nucleotide substitution and evolution in the nonstructural proteins is
limited.
Based on the VP2 sequence, CPV-2 is divided into the three variants,
CPV-2a, CPV-2b, and CPV-2c, which have recently co-circulated in dog
populations worldwide. The CPV-2a variant differs from the original
CPV-2 by five amino acid mutations (Met87Leu, Ile101Thr, Ala300Gly,
Asp305Tyr, and Val555Ile), while CPV-2b reveals a new mutation in
residue Asn426Asp. Until now, the CPV-2a and CPV-2b variants replaced
the original CPV-2 since the 1980s (Parrish et al., 1991; Parrish et
al., 1988), whereas the last variant of CPV-2, CPV-2c, firstly emerged
in Italy in 2001 (Buonavoglia et al., 2001). The CPV-2c variant has a
specific 426Glu mutation in the VP2 gene. In recent years, CPV-2c has
globally spilled over in many geographic regions and currently causes
fatal disease in both domestic and wild dog populations (Aldaz et al.,
2013; Decaro & Buonavoglia, 2012; Geng et al., 2015; Parthiban,
Mukhopadhyay, Antony, & Pillai, 2010).
The CPV-2c variant was first identified in Vietnam in 2002, which was
the first report in Asia (Nakamura et al., 2004). Later, this variant
was identified in dogs from other Asian countries, including China,
India, Taiwan, Indonesia, Laos, and Thailand (Charoenkul et al., 2019;
Chiang, Wu, Chiou, Chang, & Lin, 2016; Geng et al., 2015; Nandi,
Chidri, Kumar, & Chauhan, 2010; Vannamahaxay et al., 2017). These
recent studies have described the molecular characteristics of the VP2
gene in Asian CPV-2c, but the full-length genome characterization of
CPV-2c in Asia has not been reported. In this study, we performed
molecular and phylodynamic analyses of the full-length genome of CPV-2c
variants isolated from domestic dogs in Vietnam.