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Analysis of canine parvoviruses circulating in Australia reveals predominance of variant 2b strains and identifies feline parvovirus-like mutations in the capsid proteins
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  • Emily Kwan,
  • Maura Carrai,
  • Gianvito Lanave,
  • Jennifer Hill,
  • Kylie Parry,
  • Mark Kelman,
  • Joanne Meers,
  • Nicola Decaro,
  • Julia Beatty,
  • Vito Martella,
  • Vanessa Barrs
Emily Kwan
The University of Sydney Faculty of Science
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Maura Carrai
The University of Sydney Faculty of Science
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Gianvito Lanave
University of Bari
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Jennifer Hill
Vetpath Laboratory Services
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Kylie Parry
Northwest Vets
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Mark Kelman
The University of Sydney Faculty of Science
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Joanne Meers
The University of Queensland
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Nicola Decaro
University of Bari
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Julia Beatty
The University of Sydney Faculty of Science
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Vito Martella
University of Bari
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Vanessa Barrs
City University of Hong Kong
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Peer review status:Published

09 May 2020Submitted to Transboundary and Emerging Diseases
11 May 2020Submission Checks Completed
11 May 2020Assigned to Editor
13 May 2020Reviewer(s) Assigned
29 May 2020Review(s) Completed, Editorial Evaluation Pending
31 May 2020Editorial Decision: Revise Major
15 Jun 20201st Revision Received
16 Jun 2020Submission Checks Completed
16 Jun 2020Assigned to Editor
16 Jun 2020Reviewer(s) Assigned
08 Jul 2020Editorial Decision: Accept
29 Jul 2020Published in Transboundary and Emerging Diseases. 10.1111/tbed.13727

Abstract

Canine parvovirus (CPV) is a major enteric pathogen of dogs worldwide that emerged in the late 1970s from a feline parvovirus (FPV)-like ancestral virus. Shortly after its emergence, variant CPVs were generated by acquiring amino-acid (aa) mutations in key capsid residues, associated with biological and/or antigenic changes. This study aimed to identify CPV variants amongst Australian dogs, to gain insights into the evolution of CPV in Australia through phylogenetic analysis of these variants, and to investigate relationships between the disease and vaccination status of dogs from which isolates were collected. CPV VP2 sequences were amplified from 79 faecal samples collected from dogs with parvoviral enteritis at 20 veterinary practices in 5 Australian states. The median age at diagnosis was 4 months (range 1 to 96 months). Only 3.7% of dogs with vaccination histories had completed recommended vaccination schedules, while 49% were incompletely vaccinated and 47.2% were unvaccinated. For the first time, CPV-2b has emerged as the dominant antigenic CPV variant circulating in dogs with parvoviral enteritis in Australia, comprising 54.4% of strains, while CPV-2a and CPV-2 comprised 43.1% and 2.5% of strains. CPV-2c strains were not identified. Analysis of translated VP2 sequences revealed a vast repertoire of aa mutations. Several Australian CPV strains displayed signatures in the VP2 protein typical of Asian CPVs, suggestion introduction of CPV strains from Asia, and/or CPV circulation between Asia and Australia. Strains of CPV were identified containing aa residues typical of FPV at capsid (VP2) key positions, representing reverse mutations or residual mutations retained from CPV-2 during adaptation from an FPV-like ancestor, suggesting that evolutionary intermediates between CPV-2 and FPV are circulating in the field. Similarly, intermediates between CPV-2a-like viruses and CPV-2 were also identified. These findings help inform a better understanding of the evolution of CPV in dogs.