Genomic RNA sequence of feline coronavirus strain FCoV C1Je

Abstract

This paper reports the first genomic RNA sequence of a field strain feline coronavirus (FCoV). Viral RNA was isolated at post mortem from the jejunum and liver of a cat with feline infectious peritonitis (FIP). A consensus sequence of the jejunum-derived genomic RNA (FCoV C1Je) was determined from overlapping cDNA fragments produced by reverse transcriptase polymerase chain reaction (RT-PCR) amplification. RT-PCR products were sequenced by a reiterative sequencing strategy and the genomic RNA termini were determined using a rapid amplification of cDNA ends PCR strategy. The FCoV C1Je genome was found to be 29,255 nucleotides in length, excluding the poly(A) tail. Comparison of the FCoV C1Je genomic RNA sequence with that of the laboratory strain FCoV FIP virus (FIPV) 79-1146 showed that both viruses have a similar genome organisation and predictions made for the open reading frames and cis-acting elements of the FIPV 79-1146 genome hold true for FCoV C1Je. In addition, the sequence of the 3′-proximal third of the liver derived genomic RNA (FCoV C1Li), which encompasses the structural and accessory protein genes of the virus, was also determined. Comparisons of the enteric (jejunum) and non-enteric (liver) derived viral RNA sequences revealed 100% nucleotide identity, a finding that questions the well accepted ‘internal mutation theory’ of FIPV pathogenicity.

Genetic diversity and phylogenetic analysis of Feline Coronavirus sequences from Portugal

“…These viral variants were found within the same animal but also in samples collected from animals sharing a multi-cat environment. This finding supports the viral internal mutation theory (Dye and Siddell, 2007) and confirms the animal exposure to divergent viral strains. The significance of FCoV quasispecies had already been studied (Battilani et al, 2003) suggesting a correlation between high viral genetic diversity within the host and development of disease.…”

Feline infectious peritonitis: insights into feline coronavirus pathobiogenesis and epidemiology based on genetic analysis of the viral 3c gene

“…Moreover, FCoV antigen was detectable by immunohistology in these tissues only in cats with FIP (Kipar et al, 2006a, b), consistent with the low FECV replication activity seen in the mononuclear cells. Dye & Siddell (2007) to detect identical 3c-mutated viruses in gut and liver of a cat with FIP; this might explain the single instance in which we found a virus with mutated 3c both in FIP lesions and in the faeces (cat 12).…”

“…In particular, it has been noted that FIPV strains frequently carry mutations that inactivate the gene for 3c (Pedersen, 2009;Vennema et al, 1998), an accessory triple-spanning membrane protein with a predicted topology similar to that of SARS coronavirus 3a (Oostra et al, 2006). Loss of 3c function thus seemingly correlates with acquisition of virulence (Haijema et al, 2004;Pedersen, 2009;Vennema et al, 1998). Siddell (2007.…”

Production of IFN-γ in feline whole blood after incubation with potential T-cell epitopes of the nucleocapsid protein of feline coronavirus

“…It has been hypothesized that virulent FCoV strains arise by a genomic mutation, possibly within the 3c gene (Pedersen, 2009;Pedersen et al, 2009;Chang et al, 2010), but the mutation potentially involved in this pathogenic shift has never been identified (Kennedy et al, 2001;Rottier et al, 2005;Dye and Siddell, 2007;Lin et al, 2009). Experimental studies reported a low morbidity rate in cats inoculated with ''virulent'' FCoVs formerly classified as FIPV (Pedersen, 1987;Kipar et al, 2001;Dean et al, 2003;Kiss et al, 2004).…”