Abstract
BackgroundThere are two biotypes of feline coronavirus (FCoV): the self-limiting feline enteric coronavirus (FECV) and the feline infectious peritonitis virus (FIPV), which causes feline infectious peritonitis (FIP), a fatal disease associated with cats living in multi-cat environments. This study provides an insight on the various immune mediators detected in FCoV-positive cats which may be responsible for the development of FIP.ResultsIn this study, using real-time PCR and multiplex bead-based immunoassay, the expression profiles of several immune mediators were examined in Crandell-Reese feline kidney (CRFK) cells infected with the feline coronavirus (FCoV) strain FIPV 79–1146 and in samples obtained from FCoV-positive cats. CRFK cells infected with FIPV 79–1146 showed an increase in the expression of interferon-related genes and pro-inflammatory cytokines such as MX1, viperin, CXCL10, CCL8, RANTES, KC, MCP1, and IL8. In addition, an increase in the expression of the above cytokines as well as GM-CSF and IFNγ was also detected in the PBMC, serum, and peritoneal effusions of FCoV-positive cats. Although the expression of MX1 and viperin genes was variable between cats, the expression of these two genes was relatively higher in cats having peritoneal effusion compared to cats without clinically obvious effusion. Higher viral load was also detected in the supernatant of peritoneal effusions compared to in the plasma of FCoV-positive cats. As expected, the secretion of IL1β, IL6 and TNFα was readily detected in the supernatant of peritoneal effusions of the FCoV-positive cats.ConclusionsThis study has identified various pro-inflammatory cytokines and interferon-related genes such as MX1, viperin, CXCL10, CCL8, RANTES, KC, MCP1, IL8, GM-CSF and IFNγ in FCoV-positive cats. With the exception of MX1 and viperin, no distinct pattern of immune mediators was observed that distinguished between FCoV-positive cats with and without peritoneal effusion. Further studies based on definitive diagnosis of FIP need to be performed to confirm the clinical importance of this study.
Highlights
There are two biotypes of feline coronavirus (FCoV): the self-limiting feline enteric coronavirus (FECV) and the feline infectious peritonitis virus (FIPV), which causes feline infectious peritonitis (FIP), a fatal disease associated with cats living in multi-cat environments
An increase in viral load was detected at different time points, with the peak viral load of 1012.54 occurring at 48 hpi, while the lowest viral load was detected at 3 hpi (Table 2)
Expression profiles of immune-related genes in FIPV 79–1146-infected cells All the analyzed immune-related genes showed significant (p < 0.05) changes in expression levels at different time points following infection with FCoV strain FIPV 79– 1146. These genes were selected based on transcriptome data from our previous study on Crandell-Reese feline kidney (CRFK) cells infected with FIPV 79–1146 [14]
Summary
There are two biotypes of feline coronavirus (FCoV): the self-limiting feline enteric coronavirus (FECV) and the feline infectious peritonitis virus (FIPV), which causes feline infectious peritonitis (FIP), a fatal disease associated with cats living in multi-cat environments. Humoral response does not seem to be beneficial and could lead to the dissemination of the virus through complement activation via formation of immune complexes and vasculitis associated with type III hypersensitivity (reviewed in [1, 2]). This would lead to effusive FIP (wet form), the most commonly reported form of FIP due to the obvious sign of peritoneal effusion. The non-effusive form of FIP is associated with partial CMI response in the individual cat to contain the virus leading to the formation of granulomas containing macrophages, which could be replaced by B cells and plasma cells [10, 11]
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