ArticleJournal of feline medicine and surgery
Identification of within-host deletions in domain 0 of the spike gene of pathogenic feline coronavirus type 2 from the USA.
Article in Journal of feline medicine and surgery. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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5 authors.
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Abstract
ObjectivesFeline coronavirus (FCoV) is widely acknowledged to gain pathogenicity within the host to cause the lethal disease feline infectious peritonitis (FIP). Most FIP cases are caused by viruses in genotype 1 (FCoV-1) via an 'internal mutation' in the spike gene. Genotype 2 (FCoV-2) has risen to prominence based on the emergence of FCoV-23, a highly pathogenic novel variant from Cyprus that has a deletion in the N-terminus (domain 0) of spike. In this study, we conducted a retrospective analysis of three cases of FCoV-2 in the USA: two (cats 344 and 346) from 2013 and one (cat 597) from 2016. Cats 344 and 597 exhibited clinical signs consistent with FCoV infection for at least 2 months. The third cat (cat 346), the daughter of cat 344, was euthanized shortly after showing signs.MethodsWe collected a total of 20 tissue, fluid and fecal samples from the three cats. We characterized the FCoV-2 in these samples using whole-genome sequencing, genetic and phylogenetic analyses, and viral RNA quantification.ResultsWhole-genome sequencing revealed that the two cats exhibiting long-term signs of FCoV infection (cats 344 and 597) each had a distinct deletion in domain 0 of spike, which was present in all examined tissues. Cat 346, the daughter of cat 344, who displayed signs for only a short period, had an intact (or long) spike gene. Low RNA titers of the FCoV-2 with the short version of spike were detected in the feces of cats 344 and 597 (2.52-5.28 RNA copies/μl).Conclusions and relevanceOur data are consistent with a model whereby FCoV-2 displaying the long version of spike is transmitted between cats, whereas the short version is generated within each cat after a prolonged infection and spreads rapidly throughout the body. We suggest that the high pathogenicity of FCoV-2 is associated with an 'internal deletion' in the spike gene.
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