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SUMMARY
Feline infectious peritonitis (FIP) is a fatal infectious disease that prominently
develops in younger cats. The disease is caused by the feline coronavirus (FeCoV)
that has two different pathotypes: The feline enteric coronavirus (FECV) is more
common and it causes mild or unapparent enteritis, while feline infectious peri tonitis virus (FIPV) is responsible for the deadly systemic immune-mediated
granulomatous disease. FECV and FIPV show functional differences, the FECV
replicates mainly in intestinal epithelium and are shed in faeces, while FIPV rep licates in monocytes and cause systemic disease. The key event in the patho genesis of FIP is the effective and sustainable viral replication in monocytes of
the FIPV. It can take weeks to months for FIP to develop after the initial infection
with FeCoV. Cats persistently infected with FECV remain mostly healthy despite
their systemic infection, and they can play important role to spread the virus
among the healthy naive cats. Only 5-12% of FeCoV infected animals develop
the FIP syndrome. The development of the disease is unpredictable, and once
FIP develops, the confirmation of diagnosis is challenging in particular in the
dry form. The process of FECV-FIPV conversion and its genetic background is
not yet completely understood, though significant progress was made in the
topic in the recent years. The macrophage tropism of FIPV seems to be primary
determined by mutations in the S protein. FeCoVs must have an intact 3c gene
to be able to replicate in the intestinal epithelium and deletions of the 3c gene
may play a role in the transformation from FECV to FIPV. The newer results not
only facilitated the better understanding of the disease but also improved the
potential toolkits for prevention, diagnostic and cure. In this paper the authors
shortly summarize the history of the disease and review the latest scientific
advances in FIP research.
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