Abstract
Feline infectious peritonitis (FIP), caused by feline coronavirus (FCoV) infection, is a highly lethal disease without effective therapy and prevention. With an immune-mediated disease entity, host genetic variant was suggested to influence the occurrence of FIP. This study aimed at evaluating cytokine-associated single nucleotide polymorphisms (SNPs), i.e., tumor necrosis factor alpha (TNF-α), receptor-associated SNPs, i.e., C-type lectin DC-SIGN (CD209), and the five FIP-associated SNPs identified from Birman cats of USA and Denmark origins and their associations with the outcome of FCoV infection in 71 FIP cats and 93 FCoV infected non-FIP cats in a genetically more diverse cat populations. A promoter variant, fTNFA - 421 T, was found to be a disease-resistance allele. One SNP was identified in the extracellular domain (ECD) of fCD209 at position +1900, a G to A substitution, and the A allele was associated with FIP susceptibility. Three SNPs located in the introns of fCD209, at positions +2276, +2392, and +2713, were identified to be associated with the outcome of FCoV infection, with statistical relevance. In contrast, among the five Birman FIP cat-associated SNPs, no genotype or allele showed significant differences between our FIP and non-FIP groups. As disease resistance is multifactorial and several other host genes could involve in the development of FIP, the five genetic traits identified in this study should facilitate in the future breeding of the disease-resistant animal to reduce the occurrence of cats succumbing to FIP.Electronic supplementary materialThe online version of this article (doi:10.1186/s13567-014-0123-6) contains supplementary material, which is available to authorized users.
Highlights
Feline infectious peritonitis (FIP), a highly lethal disease with nearly 100% mortality among ill cats once clinical signs appear, is caused by feline coronavirus (FCoV) infection [1]
Polymorphism at fTNFA - 421 was found to be significantly associated with resistance to FIP Because the overproduction of TNF-α is widely reported in FIP animals and is considered to contribute to the pathogenesis of FIP, we first screened the polymorphisms at the 5′ terminus of the fTNFA gene, including the proximal regulatory region (PRR), the 5′-untranslated region (UTR), and part of exon 1, in 71 FIP and 93 control cats
One single nucleotide polymorphisms (SNPs) located in exon 1 at position +23 results in the substitution of CGG to CAG, causing an amino acid change from Arg to Gly (R8G); the remaining SNPs were found in the PRR
Summary
Feline infectious peritonitis (FIP), a highly lethal disease with nearly 100% mortality among ill cats once clinical signs appear, is caused by feline coronavirus (FCoV) infection [1]. There is currently no therapy proven to be effective for the treatment of FIP, and once diagnosis is confirmed, euthanasia is generally inevitable. This disease has been described for over fifty years [3], studies attempting to develop vaccines with different approaches have all failed due to the immunopathogenic features of infection by this virus [4]. Despite the close relationship to FCoV infection, polymorphisms in the fCD209 and feline TNF-α (fTNFA) genes and their association with FIP occurrence have never been investigated
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