Abstract
Recent evidence suggests that a mutation in the spike protein gene of feline coronavirus (FCoV), which results in an amino acid change from methionine to leucine at position 1058, may be associated with feline infectious peritonitis (FIP). Tissue and faecal samples collected post mortem from cats diagnosed with or without FIP were subjected to RNA extraction and quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR) to detect FCoV RNA. In cats with FIP, 95% of tissue, and 81% of faecal samples were PCR-positive, as opposed to 22% of tissue, and 60% of faecal samples in cats without FIP. Relative FCoV copy numbers were significantly higher in the cats with FIP, both in tissues (P < 0.001) and faeces (P = 0.02). PCR-positive samples underwent pyrosequencing encompassing position 1058 of the FCoV spike protein. This identified a methionine codon at position 1058, consistent with the shedding of an enteric form of FCoV, in 77% of the faecal samples from cats with FIP, and in 100% of the samples from cats without FIP. In contrast, 91% of the tissue samples from cats with FIP and 89% from cats without FIP had a leucine codon at position 1058, consistent with a systemic form of FCoV. These results suggest that the methionine to leucine substitution at position 1058 in the FCoV spike protein is indicative of systemic spread of FCoV from the intestine, rather than a virus with the potential to cause FIP.
Highlights
Feline coronavirus (FCoV) infection is ubiquitous in domestic cats, in multi-cat households where up to 90% of animals may be infected [1,2,3]
A total of 86 tissue samples were analysed by FCoV quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR), and 52 (60%) were positive
The most important finding in this study is that the M1058L substitution in the FCoV S protein does not correlate with feline infectious peritonitis (FIP) disease phenotype, as was proposed by Chang et al [13]
Summary
Feline coronavirus (FCoV) infection is ubiquitous in domestic cats, in multi-cat households where up to 90% of animals may be infected [1,2,3]. The virus mutates into the virulent form This form has an enhanced tropism for monocytes/macrophages, and in vitro studies suggest that this is reflected as sustainable replication in, and Currently, there is intense interest in determining which mutations alter the virulence of FCoVs. A recent paper published by Chang et al [13] derived full genome sequence data from a collection of FCoVs obtained from the faeces of healthy cats and from the tissues of cats diagnosed with FIP. A recent paper published by Chang et al [13] derived full genome sequence data from a collection of FCoVs obtained from the faeces of healthy cats and from the tissues of cats diagnosed with FIP They provided evidence of an association between FCoV virulence and an amino acid substitution (methionine to leucine at position 1058, M1058L) within the putative fusion peptide of the FCoV spike (S) protein. The S protein fusion peptide is a critical element in the fusion of viral and cellular membranes during virus entry [14] and it is reasonable to think that amino acid substitutions within this peptide may alter the tropism of the virus
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
