Perspectives on the epizootiology of feline enteric coronavirus and the pathogenesis of feline infectious peritonitis

Abstract

This review presents some current thoughts regarding the epizootiology of the feline coronaviruses; feline infectious peritonitis virus (FIPV) and feline coronavirus (FECV) with primary emphasis on the pathogenesis of these viruses in nature. Although the mechanism(s) whereby FIPV causes disease are still incompletely understood, there have been significant contributions to the literature over the past decade which provide a framework upon which plausible explanations can be postulated. Two concepts are presented which attempt to clarify the pathogenesis of FIPV and at the same time may serve as an impetus for further research. The first involves the hypothesis, originally promulgated by Pedersen in 1981, that FIPV is derived from FECV during virus replication in the gastrointestinal tract. The second involves a unique mechanism of the mucosal immune system referred to as oral tolerance, which under normal conditions promotes the production of secretory immunity and suppresses the production of systemic immunity. In the case of FIPV infection, we propose that oral tolerance is important in the control of the virus at the gastrointestinal tract level. Once oral tolerance is disrupted, FIPV is capable of systemic spread resulting in immune-mediated vasculitis and death. Thus, it may be that clinical forms of FIP are due to a combination of two events, the first being the generation of FIPV from FECV, and the second being the capacity of FIPV to circumvent oral tolerance.

Prevalence of feline coronavirus types I and II in cats with histopathologically verified feline infectious peritonitis

“…The genome of some FECV strains proved to be 0.3 kb shorter, suggesting a deletion of 300 bp at the 3 -end (Vennema et al, 1992). Molecular studies showed that FIPV arises by mutation from FECV (Pedersen et al, 1981;Evermann et al, 1991;Hök, 1993;Poland et al, 1996;Herrewegh et al, 1997;Vennema et al, 1994Vennema et al, , 1998. Both FIPV and FECV may, depending on their virulence, cause viremia (Herrewegh et al, 1995;Fehr et al, 1996;Gunn-Moore et al, 1998;Horzinek, 2000).…”

Clinical and Immunological Characteristics of Cats Affected by Feline Infectious Peritonitis

“…FeCoV are known for their considerable variability. It has been demonstrated that FIP can develop as a result of mutation of FeCoV in the intestine of cats affected by coronavirus-induced enteritis (Evermann et al 1991). Outbreaks of FIP can occur also in colonies where not a single case was recorded in the past.…”

Antigenic and Plaque Variations of Serotype II Feline Infectious Peritonitis Coronaviruses.

“…In other words, one could identify an isolate as FIPV or FECV, regardless of clinical conditions of the cat from which it was isolated, only after experimental determination of its disease-causing potential in cats. FECV is epizootiologically the predominant FCoV in the field, and it has been tentatively concluded that FIPV is a mutant of FECV, though the exact mutation mechanism has yet to be clarified [4,21,23,29].…”

“…In other words, one could identify an isolate as FIPV or FECV, regardless of clinical conditions of the cat from which it was isolated, only after experimental determination of its disease-causing potential in cats. FECV is epizootiologically the predominant FCoV in the field, and it has been tentatively concluded that FIPV is a mutant of FECV, though the exact mutation mechanism has yet to be clarified [4,21,23,29].FCoVs are divided into two distinct serotypes I and II by neutralization specificities induced by a spike protein [5,10,11,19]. Serotype I FCoV isolates have been numerically superior [22] and predominantly distributed among cats [9].…”