The biology of the feline infectious peritonitis virus (FIPV)

Feline infectious peritonitis (FIP) is a fatal infectious disease that prominently devleops in younger cats. The disease is caused by the feline coronavirus (FeCoV) that has two different pathotypes: The felline enteric coronavirus (FECV) is more common and it cause mild or unapparent enterites, while feline infectious peritonitis 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 replicates in monocytes and cause systemic disease. The key event in the pathogenesis 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 infections 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. FeCoV 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.