Chang HW, de Groot RJ, Egberink HF et al.: Feline infectious peritonitis: insights into feline coronavirus pathobiogenesis and epidemiology based on genetic analysis of the viral 3c gene, J Gen Virol 91:415, 2010.
The virus of the lethal disease, feline infectious peritonitis (FIP), is closely related to the relatively innocuous form of feline coronavirus (FCoV). There is genetic and animal experimental evidence to indicate that the disease-causing form evolves time and time again from the harmless one by mutation in individual infected cats. What this specific mutation in the virus is remains unknown. One possible gene that may be involved, termed the “3c” gene, encodes a viral protein of unknown function. Previous studies have identified mutations in this gene that may be associated with FIP development. In this report, the investigators examined the 3c gene in the coronavirus infecting 27 healthy cats and 28 cats diagnosed with FIP in order to compare the viruses in this genetic region. Interestingly, the 3c gene in the virus of healthy cats was always intact, with no mutations. However, in cats with FIP, the majority (20/28) of viruses had mutations in this gene, varying from minor changes in a few amino acids to major changes leading to lack of function of the encoded protein. The researchers also tested the feces of cats with FIP for coronavirus. Virus was found in only 6 of 17 cats, indicating that in most cats with FIP, coronavirus has been cleared from the intestines and is only present in the tissues. In samples from 6 cats in which virus were detected, the 3c gene either had no mutations (5/6) or only one amino acid change (1/6). These investigators proposed the following scenario: Cats become infected by circulating virus that replicates in the gut. Replication in this compartment and efficient fecal shedding strictly require an intact viral 3c gene. A mutation in the virus occurs continually, one or more of which incidentally provides the virus with the ability to replicate in macrophages and monocytes, which then spread the – now FIPV – infection to organs throughout the body. Once in this new environment, virus propagation no longer requires the 3c gene; thus, mutations readily occur in the gene that may even improve the virus’ replication in tissue. The result is the disease feline infectious peritonitis. [MK]Related articles:Brown MA, Troyer JL, Pecon-Slattery J et al.: Genetics and pathogenesis of feline infectious peritonitis virus, Emerg Infect Dis 15:1445, 2009.Pedersen NC: A review of feline infectious peritonitis virus infection: 1963-2008, Journal of Feline Medicine & Surgery 11:225, 2009.
feline infectious peritonitis