It has been suggested that mutations in the 3c and 7b genes may be involved in the transition to FIPV (1,12,15).
Each sample was retrieved from formalin-fixed, paraffin-embedded tissue blocks from which sections were stained by using FIPV 3-70 antibody (Custom Monoclonals, Sacramento, CA, USA).
For each category of FIPV or FECV infection, cats harboring viruses with or without mutations at the S1/S2 site were counted.
FECV and FIPV are considered independently circulating viruses by some investigators (5,6).
In contrast, FIPV is rare, but the consequences of infection are devastating.
To establish a consistent cause for a virulence shift in FCoV, specifically the predominant serotype I FCoV, we sequenced the entire genome of several FECV and FIPV specimens and then concentrated on the most conspicuous region of consistent difference by collecting and sequencing additional FECV and FIPV samples.
The relationship between FECV and FIPV has become a matter of debate.
FECV and FIPV cases were found in 7 (designated A to G); the remaining cattery (H) provided 2 cats with FIP.
Viral genetic determinants specifically associated with FIPV pathogenesis have yet to be discovered.
The in vivo mutation hypothesis of FIPV pathogenesis is widely cited, although it has never been explicitly confirmed.
Most cats naturally exposed as adults to FIPV develop antibody titers without showing clinical signs.
Together with porcine Transmissible gastroenteritis virus (TGEV), canine coronavirus, and human coronavirus 229E (HCV), the feline coronaviruses form a separate cluster within, the genus Coronavirus, including Feline enteric coronavirus, and FIPV (26).