Data regarding the molecular biology of feline coronaviruses

The authors give a short review on contemporary knowledge about the molecul ar biology of feline coronaviruses, Particular attention is paid to the con nection between feline enteric coronaviruses (FECV) and feline infectious p eritonitis viruses (FIPV). FIP is a leading infectious cause of death among young cats, and occurs wor ldwide. The disease has a progressive immune-mediated pathogenesis. Diagnos is and control of the disease is difficult since serological investigations are not informative for this purpose, and neither treatment nor reliable v accines are available at present. Based on in vitro neutralisation, the existence of two serotypes of feline coronaviruses has been shown. They differ mainly in their field prevalence and their in vitro growth characteristics. Feline coronaviruses were divide d into two biotypes on the grounds of pathogenicity, ie. FECV and FIP virus es. FECV may produce mild enteritis, but most infections remain subclinical . However, FECV presents a considerable health risk to cats because It is t he precursor of FIPV. FECV can establish persistent infection in cats during natural infection. A symptomatic FECV-infected carrier cats spread the infection to susceptible animals via the fecal-oral route. FIP viruses arise as a result of deletion s and presumably mutations in the FECV genome during the intestinal replica tive phase of infection. Deletions occur most specifically in the ORF3c reg ion of the FECV genome. The intact ORF3c presumably suppresses the function of the virulence factor ORF7b in FECVs. However, in their changed FIPV cou nterparts, where the ORF3c is deleted or truncated, this suppression does n ot function, therefore the ORF7b may readily contribute to the invasion of the organism and to the development of FIP. In experimentally infected Eats, the authors found that the persisting FECV forms in the large intestine a quasi-species population the composition of which varies with time. The changes affect the structural-protein coding r egions of the viruses. Having entered the different organs, this variabilit y is markedly reduced, which is probably due to strong selection. Furthermo re, since some of the detected viruses were partly or entirely lacking ORF7 b, the existence of other virulence factors cannot be excluded, Thus, the incidence of FIP in a cat population is not the result of the cir culation of certain FIP viruses, but rather it is in strict correlation wit h the mutation rate of FECV to FIPV. Therefore, to learn the probability of occurrence of FIP viruses and the di sease itself, it is recommended to monitor a population for the prevalence of the asymptomatic FECV carriers. We suggest using RT-PCR targeting one of the most conservative genomic regions for this purpose. However, the regio ns ORF3c and ORF7b that are presumably responsible for the evolution of FIP viruses should be also scrutinised in pathogenicity studies. Similarly, th e molecular background of natural resistance of some cat breeding-lines aga inst feline coronaviruses would be also well worth investigating.