Feline infectious peritonitis (FIP) belongs to the few animal virus diseases in 
which, in the course of a generally harmless persistent infection, a virus 
acquires a small number of mutations that fundamentally change its 
pathogenicity, invariably resulting in a fatal outcome. The causative agent of 
this deadly disease, feline infectious peritonitis virus (FIPV), arises from 
feline enteric coronavirus (FECV). The review summarizes our current knowledge 
of the genome and proteome of feline coronaviruses (FCoVs), focusing on the 
viral surface (spike) protein S and the five accessory proteins. We also review 
the current classification of FCoVs into distinct serotypes and biotypes, 
cellular receptors of FCoVs and their presumed role in viral virulence, and 
discuss other aspects of FIPV-induced pathogenesis. Our current knowledge of 
genetic differences between FECVs and FIPVs has been mainly based on comparative 
sequence analyses that revealed "discriminatory" mutations that are present in 
FIPVs but not in FECVs. Most of these mutations result in amino acid 
substitutions in the S protein and these may have a critical role in the switch 
from FECV to FIPV. In most cases, the precise roles of these mutations in the 
molecular pathogenesis of FIP have not been tested experimentally in the natural 
host, mainly due to the lack of suitable experimental tools including 
genetically engineered virus mutants. We discuss the recent progress in the 
development of FCoV reverse genetics systems suitable to generate recombinant 
field viruses containing appropriate mutations for in vivo studies.