Feline infectious peritonitis (FIP) is now the leading cause of irreversible virally induced mortality among domestic cats worldwide. The feline corona virus presents itself as two distinct and gravely opposite pathologies. The first and primary pathology is caused by Feline Enteric Coronavirus (FeCoV, FECV), which causes a mild or unapparent gastrointestinal infection of the columnar epithelial cells that line the intestines within the cat. The second pathology is caused by Feline Infectious Peritonitis Virus (FIPV), which leads to the lethal hyperimmune inflammatory condition known as Feline Infectious Peritonitis (FIP). Worldwide, public animal shelters house cats and kittens that are exposed to this and other feline viruses, raising the prevalence of feline coronavirus to 100% exposure for all shelter cats and kittens. This virus is also prevalent within the large cat populations of the world, with fatal outcomes for most exposed Cheetahs, who are nearly 100% identical genetically. The course of the first pathology, FeCoV infection, is self-limiting and resolves without further incident for approximately 90% of the domestic cat and kitten population. For the remaining 10% of cats and kittens, the FeCoV ventures beyond the columnar epithelial cells of the feline intestines, then succeeds in entering and propagating within the monocytes and macrophages (immune system cells) causing an irreversible and fatal hyperimmune cascade of inflammation. At this cell tropism-specific turning point, the virus is called FIPV. Several research groups have attempted to identify the differences in genetic structure, as well as the pathological mechanisms of the two feline coronavirus biotypes, FeCoV and FIPV. There is controversy regarding whether the two virus biotypes are one in the same, differing by one or two amino acids in the S-spike protein on the viral exterior coat, or that they are two distinct strains in which FeCoV mutates within the feline host to become the lethal FIP biotype. Our retrospective clinical data indicates that FIPV and FeCoV are the same virus. Our flow cytometry and MALDI mass spectrometry data was limited to successful isolation of feline leukocytes, but further study is planned to identify the actual cellular proteins.