Abstract

To evaluate the most controversial issue concerning current feline coronavirus (FCoV) virology, the coexisting hypotheses of the intrahost and interhost origins of feline infectious peritonitis virus (FIPV) in regard to the pathogenesis of feline infectious peritonitis (FIP), this study aimed to assess the molecular diversity of the membrane gene FCoVs in 190 samples from 10 cats with signs of FIP and in 5 faecal samples from cats without signs of FIP. All samples from the non-FIP cats and 25.26% of the samples from the FIP cats were positive for the FCoV membrane (M) gene. Mutations in this gene consisted of SNP changes randomly scattered among the sequences; few mutations resulted in amino acid changes. No geographic pattern was observed. Of the cats without FIP that harboured FECoV, the amino acid sequence identities for the M gene were 100% among cats (Cats 1–3) from the same cattery, and the overall sequence identity for the M gene was ≥91%. In one cat, two different lineages of FCoV, one enteric and one systemic, were found that segregated apart in the M gene tree. In conclusion, the in vivo mutation transition hypothesis and the circulating high virulent-low virulent FCoV hypothesis have been found to be plausible according to the results obtained from sequencing the M gene.

Highlights

  • Feline coronavirus (FCoV), a widespread pathogen of domestic cat populations worldwide, is an enveloped singlestranded RNA virus of the order Nidovirales, family Coronaviridae, subfamily Coronavirinae, genus Alphacoronavirus, species alphacoronavirus 1

  • Feline infectious peritonitis (FIP), a possible complication of FCoV infection in a small proportion of cats, is a lethal, systemic immune-mediated disease caused by a second FCoV pathotype, feline infectious peritonitis virus (FIPV) [1, 2]

  • To evaluate the most controversial issue concerning current FCoV virology, the coexisting hypotheses of the intrahost and interhost origins of FIPV in regard to FIP pathogenesis and to gain more insight into FCoV evolution, this study aimed to assess the molecular diversity of FCoVs in multiple organs of cats with signs of FIP and in faecal samples from cats without signs of FIP

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Summary

Introduction

Feline coronavirus (FCoV), a widespread pathogen of domestic cat populations worldwide, is an enveloped singlestranded RNA virus of the order Nidovirales, family Coronaviridae, subfamily Coronavirinae, genus Alphacoronavirus, species alphacoronavirus 1. Most infections are either asymptomatic or result in a mild, self-limiting gastrointestinal disease, and, in these cases, the causative agent is the feline enteric coronavirus (FECoV) pathotype. Feline infectious peritonitis (FIP), a possible complication of FCoV infection in a small proportion of cats, is a lethal, systemic immune-mediated disease caused by a second FCoV pathotype, feline infectious peritonitis virus (FIPV) [1, 2]. Specific genetic determinants of these clinical outcomes have yet to be discovered in cats. This disease is one of the most serious viral infections in cats, because of its fatal nature and because of the difficulties in diagnosing FIP antemortem and in controlling the spread of FCoV [5]

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