Abstract
Feline panleukopenia is a severe disease of cats caused by feline parvovirus (FPV), and marginally canine parvovirus (CPV). Despite being less rapid than CPV, FPV evolution deserves attention, especially since outbreaks of particular severity are currently reported. This apparently different virulence needs monitoring from genetic and clinical points of view. This manuscript explored FPV molecular epidemiology at both Italian and international levels and the possible association between viral phylogeny and disease severity. Sequences from clinical cases of feline panleukopenia in Italy were obtained from 2011 to 2019, and the etiological agent was characterized, distinguishing FPV from CPV. Phylogenetic and phylodynamic analyses were conducted on Italian and international sequences. Moreover, the association between the viral sequence and clinical variables was evaluated on a group of highly characterized patients. After its origin in the 1920s, FPV showed a constant population size until a more recent expansion since 2000. Few long-distance introduction events characterized FPV spreading, however, most of its evolution occurred locally. Although without a strong statistical association, several clinical variables appeared influenced by viral phylogeny, suggesting a differential virulence potentially characterizing FPV strains. These results stress the importance of the continuous study of viral evolution and its repercussions on the disease clinical aspects.
Highlights
Carnivore protoparvovirus 1 is a recently defined species, which groups several wellknown viruses as canine parvovirus (CPV) and feline parvovirus (FPV) [1], among others.These two viruses share close antigenic, phylogenetic, and evolutive relationships and cause gastroenteric disease and immunosuppression in young animals [2].Since its panzootic emergence in the late 1970s [3], CPV has long drawn remarkable attention as one of the best characterized and most studied cases of multiple host jump.Despite its likely origin from FPV [4], CPV-2, as initially named, was able to infect only dogs and later, through a rapid evolution, new phenotypic variants were discovered that regained the capability of infecting cats [5]
FPV is known since the early 20th century [7], it showed a constant viral population size and lower evolutionary rate [8] and its genetic variability was driven mainly by genetic drift [6]
The present study aimed to provide a comprehensive picture of the association between viral features, epidemiology, and host response
Summary
Carnivore protoparvovirus 1 is a recently defined species, which groups several wellknown viruses as canine parvovirus (CPV) and feline parvovirus (FPV) [1], among others.These two viruses share close antigenic, phylogenetic, and evolutive relationships and cause gastroenteric disease and immunosuppression in young animals [2].Since its panzootic emergence in the late 1970s [3], CPV has long drawn remarkable attention as one of the best characterized and most studied cases of multiple host jump.Despite its likely origin from FPV [4], CPV-2, as initially named, was able to infect only dogs and later, through a rapid evolution, new phenotypic variants were discovered that regained the capability of infecting cats [5]. Carnivore protoparvovirus 1 is a recently defined species, which groups several wellknown viruses as canine parvovirus (CPV) and feline parvovirus (FPV) [1], among others. These two viruses share close antigenic, phylogenetic, and evolutive relationships and cause gastroenteric disease and immunosuppression in young animals [2]. Despite its likely origin from FPV [4], CPV-2, as initially named, was able to infect only dogs and later, through a rapid evolution, new phenotypic variants were discovered that regained the capability of infecting cats [5]. FPV has remained more stable instead, both in variability and host range [6]. FPV has been slightly more neglected than its conspecific CPV
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