Introduction

Canine parvovirus (CPV), aCarnivore Protoparvovirus 1 virus in theParvoviridae family, is a non-enveloped, single-stranded DNA virus, that is one of the most common enteric viral pathogens of domestic dogs (Hoelzer & Parrish, 2010; D. Wang, Yuan, Davis, & Parrish, 1998). The 5.2 kb genome contains two major open reading frames, ORF1 and ORF2, which encode non-structural proteins NS1 and NS2, and viral proteins VP1 and VP2, respectively (Tsao et al., 1991).
When CPV emerged in 1978 as a new virus infecting dogs it caused a severe disease panzootic among domestic and wild dogs (Canis familiaris ) with clinical signs including fever, vomiting and haemorrhagic diarrhoea, as well as myocarditis in young puppies (N. Decaro & Buonavoglia, 2012; Hoelzer & Parrish, 2010). The virus was named CPV-2 to distinguish it from Canine bocaparvovirus (also known as minute virus of canines or CPV-1), the first parvovirus discovered in dogs (Binn, Lazar, Eddy, & Kajima, 1970). Within a few years, CPV-2 was replaced in the field by a new antigenic variant with greater fitness in dogs called CPV-2a (426-Asp), while two other variants CPV-2b (426-Asn) and CPV-2c (426-Gly) emerged in 1984 (Parrish et al., 1991) and 1996 (Decaro et al., 2007), respectively. These three variants differ from CPV-2 at five VP2 amino acid (aa) residues (Met-87-Leu, Ile-101-Thr, Ala-300-Gly, Asp-305-Tyr and Asn-375-Asp) and from each other by a single aa substitution at position 426 (Parrish et al., 1988; Shackelton, Parrish, Truyen, Holmes, & Berns, 2005; Truyen, Evermann, Vieler, & Parrish, 1996). While the 426 substitution makes each variant antigenically distinct, phylogenetically they lack monophyletic segregation and form a clade of “CPV-2a-like” viruses distinct from the original CPV-2 virus (Voorhees et al., 2019).
The relative frequencies of CPV antigenic variants differ between countries, because, although the emergence of CPV-2a was followed by global spread, there have been no global sweeps of CPV-2b or CPV-2c (Voorhees et al., 2019). Further, the distribution of variants is not static, as illustrated by molecular surveillance in Argentina, where CPV-2c was the predominant strain circulating in 2006, but in 2010 a novel CPV-2a strain emerged and rapidly became dominant (Maya et al., 2013).
In Australia, CPV was first detected in 1978 (Colin R. Parrish et al., 1988). Molecular surveillance carried out between 1980 and 2005 showed a clear predominance of CPV-2a, which comprised 95% of isolates from dogs with parvoviral enteritis (Meers, Kyaw-Tanner, Bensink, & Zwijnenberg, 2007). Molecular analysis of isolates from 2007 to 2016, demonstrated that CPV-2b strains comprised 46.5% of isolates, while CPV-2a remained predominant (53.5%) (Clark et al., 2017). In 2017, CPV-2c was reportedly detected for the first time in Australia, from three isolates collected in 2015 from domestic dogs with parvoviral enteritis (Woolford et al., 2017).
This study aimed to identify and analyse CPV variants and their VP2 capsid mutations amongst Australian dogs, to gain insights into the evolution of CPV in Australia and to investigate relationships between the disease and vaccination status of dogs from which isolates were collected.