Abstract

Canine parvovirus (CPV) disease is an acute, highly infectious disease threatening the dog-raising industry. So far there are no effective therapeutic strategies to control this disease. Although the canine transferrin receptor (TfR) was identified as a receptor for CPV infection, whether extracellular domain of TfR (called soluble TfR (sTfR)) possesses anti-CPV activities remains elusive. Here, we used the recombinant sTfR prepared from HEK293T cells with codon-optimized gene structure to investigate its anti-CPV activity both in vitro and in vivo. Our results indicated that codon optimization could significantly improve sTfR expression in HEK293T cells. The prepared recombinant sTfR possessed a binding activity to both CPV and CPV VP2 capsid proteins and significantly inhibited CPV infection of cultured feline F81 cells and decreased the mortality of CPV-infected dogs, which indicates that the sTfR has the anti-CPV activity both in vitro and in vivo.

Highlights

  • Canine parvovirus (CPV) was first identified in 1978 as a pathogen that is responsible for serious gastroenteritis and myocarditis in dogs [1]

  • Based on the interaction between CPV and transferrin receptor (TfR), we proposed that canine extracellular domain of TfR, called soluble TfR, might have the anti-CPV activities

  • We investigated whether recombinant soluble TfR (sTfR) has the ability to block the CPV infection

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Summary

Introduction

Canine parvovirus (CPV) was first identified in 1978 as a pathogen that is responsible for serious gastroenteritis and myocarditis in dogs [1]. There are mainly three antigenic types of CPV (CPV-2a, CPV-2b, and CPV-2c) that are prevalent in different countries and cause major infectious disease threatening dog-raising industry. CPV is a small nonenveloped, single-stranded DNA virus [2,3,4]. The linear single-strand DNA genome, about 5 kb long, contains two open reading frames (ORFs). VP2 (426 amino acid residues) is the main component in CPV capsid which possesses strong antigenic properties. The canine transferrin receptor (TfR) has been identified as a receptor for CPV infection mediated by VP2-TfR interaction [5,6,7]

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