Abstract

Feline Infectious Peritonitis (FIP)—the deadliest infectious disease of young cats in shelters or catteries—is induced by highly virulent feline coronaviruses (FCoVs) emerging in infected hosts after mutations of less virulent FCoVs. Previous studies have shown that some mutations in the open reading frames (ORF) 3c and 7b and the spike (S) gene have implications for the development of FIP, but mainly indirectly, likely also due to their association with systemic spread. The aim of the present study was to determine whether FCoV detected in organs of experimentally FCoV infected healthy cats carry some of these mutations. Viral RNA isolated from different tissues of seven asymptomatic cats infected with the field strains FCoV Zu1 or FCoV Zu3 was sequenced. Deletions in the 3c gene and mutations in the 7b and S genes that have been shown to have implications for the development of FIP were not detected, suggesting that these are not essential for systemic viral dissemination. However, deletions and single nucleotide polymorphisms leading to truncations were detected in all nonstructural proteins. These were found across all analyzed ORFs, but with significantly higher frequency in ORF 7b than ORF 3a. Additionally, a previously unknown homologous recombination site was detected in FCoV Zu1.

Highlights

  • Feline Coronaviruses (FCoVs) are endemic in the domestic cat population and are found worldwide with high seroprevalences

  • Based on the hypothesis that certain mutations are essential for the capacity of feline coronaviruses (FCoVs) to spread systemically, the present study investigated a cohort of systemically infected healthy carrier cats at different time points post experimental infection for the presence of a range of mutations in the genes encoding for the S protein, nonstructural/accessory proteins (NSP) 3abc, and NSP 7b, which have been shown to have implications for the development of Feline Infectious Peritonitis (FIP)

  • To track viral sequence mutations in organs of healthy FCoV carrier cats, we investigated FCoV

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Summary

Introduction

Feline Coronaviruses (FCoVs) are endemic in the domestic cat population and are found worldwide with high seroprevalences. Due to infidelity of the RNA polymerase, FCoVs show high mutation rates upon replication. This leads to the formation of quasispecies, a cloud-like appearance of multiple genetic virus variants that are linked by mutations [2,3]. Virus variants that acquire high virulence can lead to Feline Infectious Peritonitis (FIP), an immune-mediated disease that is currently the most frequent fatal infectious disease in young pedigree cats and cats in shelters [4,5]. The pathogenesis of FIP is still not fully understood [6]

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