Significance of Coronavirus Mutants in Feces and Diseased Tissues of Cats Suffering from Feline Infectious Peritonitis

Niels C Pedersen,Kimberly A Dodd,Hongwei Liu,Patricia A Pesavento

doi:10.3390/v1020166

Abstract

The internal FECV→FIPV mutation theory and three of its correlates were tested in four sibs/half-sib kittens, a healthy contact cat, and in four unrelated cats that died of FIP at geographically disparate regions. Coronavirus from feces and extraintestinal FIP lesions from the same cat were always >99% related in accessory and structural gene sequences. SNPs and deletions causing a truncation of the 3c gene product were found in almost all isolates from the diseased tissues of the eight cats suffering from FIP, whereas most, but not all fecal isolates from these same cats had intact 3c genes. Other accessory and structural genes appeared normal in both fecal and lesional viruses. Deliterious mutations in the 3c gene were unique to each cat, indicating that they did not originate in one cat and were subsequently passed horizontally to the others. Compartmentalization of the parental and mutant forms was not absolute; virus of lesional type was sometimes found in feces of affected cats and virus identical to fecal type was occasionally identified in diseased tissues. Although 3c gene mutants in this study were not horizontally transmitted, the parental fecal virus was readily transmitted by contact from a cat that died of FIP to its housemate. There was a high rate of mutability in all structural and accessory genes both within and between cats, leading to minor genetic variants. More than one variant could be identified in both diseased tissues and feces of the same cat. Laboratory cats inoculated with a mixture of two closely related variants from the same FIP cat developed disease from one or the other variant, but not both. Significant genetic drift existed between isolates from geographically distinct regions of the Western US.

Highlights

Feline infectious peritonitis (FIP) was first introduced as an “important disorder of cats” by Holzworth [1] and a clinico-pathologic conference on the disease was published the following year [2].The incidence of FIP rose progressively over the two decades
Structural and accessory genes of Feline coronavirus from the feces and diseased tissues of cats with FIP are virtually identical with the exception of truncating mutations in the 3c gene
Among all of the genes sequenced, only the 3c genes of the FIP virus (FIPV) isolates had SNPs that resulted in premature stop codons or deletions that caused frame shifts; both resulting in a variable truncation of the 3c protein (Figure 2)

Summary

Introduction

Feline infectious peritonitis (FIP) was first introduced as an “important disorder of cats” by Holzworth [1] and a clinico-pathologic conference on the disease was published the following year [2].The incidence of FIP rose progressively over the two decades. Feline infectious peritonitis (FIP) was first introduced as an “important disorder of cats” by Holzworth [1] and a clinico-pathologic conference on the disease was published the following year [2]. The incidence is several times higher among kittens and young cats originating from catteries or shelters. The disease was thought to be viral when first described but no specific etiologic agent was identified at the time [4]. Zook et al [5] observed virus particles in the tissues of experimentally infected cats, the close similarities of FIP virus (FIPV) in tissues to members of the family Coronaviridae was noted by Ward [6]. The existence of two serotypes, feline- or canine-coronavirus like, was described in

Objectives

Results

Conclusion