<p>Cross-species transmission of coronaviruses (CoVs) poses a serious threat to both animal and human health<sup><CitationRef AdditionalCitationIDS="CR2" CitationID="CR1">1</CitationRef>–<CitationRef CitationID="CR3">3</CitationRef></sup>. While the large RNA genome of CoVs shows relatively low mutation rates, recombination within genera is frequently observed<sup><CitationRef AdditionalCitationIDS="CR5 CR6" CitationID="CR4">4</CitationRef>–<CitationRef CitationID="CR7">7</CitationRef></sup>. Companion animals are often overlooked in the transmission cycle of viral diseases; however, the close relationship of feline (FCoV) and canine CoV (CCoV) to human hCoV-229E<sup><CitationRef CitationID="CR5">5</CitationRef>,<CitationRef CitationID="CR8">8</CitationRef></sup>, as well as the susceptibility of these animals to&#xa0;SARS-CoV-2<sup><CitationRef CitationID="CR9">9</CitationRef></sup>, highlight their importance in potential transmission cycles. While recombination between CCoV and FCoV of a large fragment spanning <i>orf1b</i> to <i>M</i> has been previously described<sup><CitationRef CitationID="CR5">5</CitationRef>,<CitationRef CitationID="CR10">10</CitationRef></sup>, here we report the emergence of a highly pathogenic FCoV–CCoV recombinant responsible for a rapidly spreading outbreak of feline infectious peritonitis (FIP) originating in Cyprus<sup><CitationRef CitationID="CR11">11</CitationRef></sup>. The minor recombinant region, spanning spike (<i>S</i>), shows 96.5% sequence identity to the pantropic canine coronavirus NA/09. Infection has rapidly spread, infecting cats of all ages. Development of FIP appears to be very frequent and sequence identities of samples from cats in different districts of the island are strongly supportive of direct transmission. A near-cat-specific deletion in the domain 0 of <i>S</i> is present in more than 90% of cats with FIP. It is unclear as yet whether this deletion is directly associated with disease development, and it may be linked to a biotype switch<sup><CitationRef CitationID="CR12">12</CitationRef></sup>. The domain 0 deletion and several amino acid changes in S, particularly the receptor-binding domain, indicate potential changes to receptor binding and cell tropism.</p>

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Feline infectious peritonitis epizootic caused by a recombinant coronavirus

  • Charalampos Attipa,
  • Amanda S. Warr,
  • Demetris Epaminondas,
  • Marie O’Shea,
  • Andrew J. Hanton,
  • Sarah Fletcher,
  • Alexandra Malbon,
  • Maria Lyraki,
  • Rachael Hammond,
  • Alexandros Hardas,
  • Antria Zanti,
  • Stavroula Loukaidou,
  • Michaela Gentil,
  • Danielle Gunn-Moore,
  • Samantha J. Lycett,
  • Stella Mazeri,
  • Christine Tait-Burkard

摘要

Cross-species transmission of coronaviruses (CoVs) poses a serious threat to both animal and human health13. While the large RNA genome of CoVs shows relatively low mutation rates, recombination within genera is frequently observed47. Companion animals are often overlooked in the transmission cycle of viral diseases; however, the close relationship of feline (FCoV) and canine CoV (CCoV) to human hCoV-229E5,8, as well as the susceptibility of these animals to SARS-CoV-29, highlight their importance in potential transmission cycles. While recombination between CCoV and FCoV of a large fragment spanning orf1b to M has been previously described5,10, here we report the emergence of a highly pathogenic FCoV–CCoV recombinant responsible for a rapidly spreading outbreak of feline infectious peritonitis (FIP) originating in Cyprus11. The minor recombinant region, spanning spike (S), shows 96.5% sequence identity to the pantropic canine coronavirus NA/09. Infection has rapidly spread, infecting cats of all ages. Development of FIP appears to be very frequent and sequence identities of samples from cats in different districts of the island are strongly supportive of direct transmission. A near-cat-specific deletion in the domain 0 of S is present in more than 90% of cats with FIP. It is unclear as yet whether this deletion is directly associated with disease development, and it may be linked to a biotype switch12. The domain 0 deletion and several amino acid changes in S, particularly the receptor-binding domain, indicate potential changes to receptor binding and cell tropism.