Abstract
Feline infectious peritonitis is a devastating, fatal disease of domestic cats caused by a pathogenic mutant virus derived from the ubiquitous feline enteric coronavirus (FECV). Infection by FECV is generally subclinical, and little is known about the mucosal immune response that controls and eliminates the virus. We investigated the mucosal immune response against FECV in an endemically infected breeding colony over a seven-month period. Thirty-three cats were grouped according to FECV seropositivity and fecal virus shedding into naïve/immunologically quiescent, convalescent and actively infected groups. Blood, fecal samples and colon biopsies were collected to assess the mucosal and systemic immunologic and virologic profile. Results showed that cats with active FECV infections have strong systemic IgG and mucosal IgA responses that wane after virus clearance. Significant FECV-specific mucosal T cell IFNγ responses were not detected in any of the three groups. A shift toward an inflammatory state in the mucosa was suggested by increased IL17:FoxP3 expression. However, no histologic abnormalities were observed, and no shifts in lymphocyte subpopulation phenotype or proliferation were noted. Together, the results suggest that control of FECV is mediated by humoral mucosal and systemic responses and that perturbations in the primary reservoir organ (colon) are minimal.
Highlights
Feline infectious peritonitis remains intractable with regard to diagnosis, treatment and prevention
Thirty-three domestic shorthair cats maintained in a specific pathogen-free (SPF) breeding colony at Colorado State University were used in the study
The feline coronavirus (FCoV) infection status of each cat included in this study was determined by an ELISA for
Summary
Feline infectious peritonitis remains intractable with regard to diagnosis, treatment and prevention (reviewed in [1,2]). It is generally accepted that feline infectious peritonitis virus (FIPV) emerges in individual cats due to the mutation of replicating feline enteric coronavirus (FECV) [2]. FECV is mucosally transmitted, replicates to the greatest levels in the intestinal tract, and most commonly persists in the colonic epithelium [3,4]. While some cats are able to control FECV replication and eliminate the infection, others remain infected and are intermittent or persistent virus shedders [5,6,7]. Within FECV-infected cats, the combination of high virus replication and high error rate in RNA replication results in innumerable mutations. If a mutation occurs that allows the virus to escape immune surveillance and efficiently infect and replicate in monocytes, it can Viruses 2019, 11, 906; doi:10.3390/v11100906 www.mdpi.com/journal/viruses
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