Cats get an enteric coronavirus which has little or no signs, but, in certain young cats, it becomes disseminated, causing peritonitis with lethality, usually 100%. Cell-mediated immunity provides an effective immune response that resolves the infection in the enteric, intestinal form. If it does not, a strong humoral response kicks in and selects for a more pathogenic form of the virus which infects and replicates in macrophages https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7112361/pdf/main.pdf. Also, autoantibodies form. There seems to be genetic predisposition toward this resulting in peritonitis https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2819880/. Peritonitis pathology involves severe systemic inflammatory damage of serosal membranes and widespread pyogranulomatous lesions in the lungs, liver, lymph tissue, and brain. The clinical finding of hypergamma-globulinemia-associated feline infectious peritonitis is indicative of over production of antibody against an antigen which cannot be cleared, allowing time for viral mutations that allow the virus to escape elimination. Therefore, like COVID-19, the feline coronavirus virus disease has this dichotomy, based on viral dissemination and autoantibodies. The right antigen for the right vaccine must be selected to prevent such adverse effects.
A new paper supports the hypothesis that immunosurveillance that reacts robustly but inadequately leads to persistent FIP virus infections and immunoselection of a strain with a shorter spike protein, more pathogenic but that is shed less. The rise of a transmissible highly pathogenic strain in Cyprus may indicate an ominous change in the epidemiology of this virus but could also be a result of the special circumstances of an island and highly populated (cats) environment. The paper states,
“Most FIP cases are caused by viruses in genotype 1 (FCoV-1) ‘internal mutation’ in the spike gene. Genotype 2 (FCoV-2) has risen to prominence based on the emergence of FCoV-23, a highly pathogenic novel variant from Cyprus that has a deletion in the N-terminus (domain 0) of spike….data are consistent with a model whereby FCoV-2 displaying the long version of spike protein is transmitted between cats, whereas the short version is generated within each cat after a prolonged infection and spreads rapidly throughout the body. We suggest that the high pathogenicity of FCoV-2 is associated with an ‘internal deletion’ in the spike gene.” Olarte-Castillo XA, Schlecht AB, Sams KL, Goodman LB, Whittaker GR. Identification of within-host deletions in domain 0 of the spike gene of pathogenic feline coronavirus type 2 from the USA. J Feline Med Surg. 2026 Jan-Dec;28(4):1098612X261433664. doi: 10.1177/1098612X261433664. Epub 2026 Mar 6. PMID: 41792121; PMCID: PMC13129309.
Global Biosurveillance 