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.