Feline infeectieuze peritonitis (FIP) is caused by a feline coronavirus (FCoV) and is one of the leading causes of death in cats nurseries and shelters that huge animal, financial and emotional losses entails FCoVs occur in two virulence variants or pathotypes which the pathogenic power is determined by their cell tropism. The feline enteric coronavirus (FECV) has a tropism for intestinal epithelial cells, called enterocytes. FECV present is endemic in cats horticulture and animal shelters, but it should be noted since it rarely intestinal infection often subclinical expires or only mild symptoms (loss of appetite, and / or mild diarrhea) gives [1-5]. The importance of FECV, however, lies in the fact that, in 5-12% of these cats virulent variants arise by mutations in the FECV genome [1]. These virulence variant, the feline infectious peritonitis virus (FIPV), are enterocypt loses tropism but has in contrast to FECV the capacity to multiply unrestrained in monocytes / macrophages [6-8], which results in a progressive, fatal, pyogranulomatous serositis and casculitis known as FIP. To win the fight against FIP, we should be able to 1) identify FCoV negative animals into the FOK, 2) identify FIP cats before the occurrence fatal tissue damage, and 3) the FIP cats to treat. To enable this approach, we must have good diagnostic testing and treatment. Both are lacking to date and can only be achieved if we knew what exactly makes the difference between FECV and FIPV.Het viral spike protein is an important determinant of cell tropism and there is speculation that mutations in the spike protein in question would be the enterocyte monocyte switch during the development of FIP [9-11], but until now could not be proven yet. Because these viruses could not be grown in cell cultures, the studies were so far are limited to genome analysis and comparisons of manure and tissue strains of FCoV infected animals.