Mutations of 3c and spike protein genes correlate with the occurrence of feline infectious peritonitis

• Published in: Veterinary microbiology Vol. 173; no. 3-4; pp. 177 - 188
• Main Authors: Bank-Wolf, Barbara Regina, Stallkamp, Iris, Wiese, Svenja, Moritz, Andreas, Tekes, Gergely, Thiel, Heinz-Jürgen
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 10.10.2014
• Subjects: 3C Viral Proteases; Accessory genes; Animals; Base Sequence; Cats; Cloning, Molecular; Coronavirus, Feline - genetics; Cysteine Endopeptidases - genetics; DNA Primers - genetics; Feces - virology; FECV; Feline coronavirus; Feline Infectious Peritonitis - virology; FIPV; Molecular Sequence Data; Mutation - genetics; Reverse Transcriptase Polymerase Chain Reaction - veterinary; Sequence Analysis, DNA - veterinary; Spike Glycoprotein, Coronavirus - genetics; Spike protein gene; Viral Fusion Proteins - genetics; Viral Proteins - genetics; Feline coronavirus; Accessory genes; FIPV; FECV; Spike protein gene
• ISSN: 0378-1135; 1873-2542
• DOI: 10.1016/j.vetmic.2014.07.020

•Sequence comparison of FIPV/FECV.•ORF3c genes of FIP animals heavily affected by nucleotide deletions/point mutations.•Genes encoding 3a, 3b, 7a and 7b displayed no mutations linked to the FCoV biotype.•Mutated 3c genes were found in ascites and faeces samples of FIP animals.•Slightly affected 3c genes were accompanied by mutations in S gene. The genes encoding accessory proteins 3a, 3b, 3c, 7a and 7b, the S2 domain of the spike (S) protein gene and the membrane (M) protein gene of feline infectious peritonitis virus (FIPV) and feline enteric coronavirus (FECV) samples were amplified, cloned and sequenced. For this faeces and/or ascites samples from 19 cats suffering from feline infectious peritonitis (FIP) as well as from 20 FECV-infected healthy cats were used. Sequence comparisons revealed that 3c genes of animals with FIP were heavily affected by nucleotide deletions and point mutations compared to animals infected with FECV; these alterations resulted either in early termination or destruction of the translation initiation codon. Two ascites-derived samples of cats with FIP which displayed no alterations of ORF3c harboured mutations in the S2 domain of the S protein gene which resulted in amino acid exchanges or deletions. Moreover, changes in 3c were often accompanied by mutations in S2. In contrast, in samples obtained from faeces of healthy cats, the ORF3c was never affected by such mutations. Similarly ORF3c from faecal samples of the cats with FIP was mostly intact and showed only in a few cases the same mutations found in the respective ascites samples. The genes encoding 3a, 3b, 7a and 7b displayed no mutations linked to the feline coronavirus (FCoV) biotype. The M protein gene was found to be conserved between FECV and FIPV samples. Our findings suggest that mutations of 3c and spike protein genes correlate with the occurrence of FIP.