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Emerg Infect Dis. 2013 Jul;19(7):1066-73. doi: 10.3201/eid1907.121094.

Mutation in spike protein cleavage site and pathogenesis of feline coronavirus.

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1
Cornell University College of Veterinary Medicine,Ithaca, New York 14853, USA.

Abstract

Feline coronaviruses (FCoV) exist as 2 biotypes: feline enteric coronavirus (FECV) and feline infectious peritonitis virus (FIPV). FECV causes subclinical infections; FIPV causes feline infectious peritonitis (FIP), a systemic and fatal disease. It is thought that mutations in FECV enable infection of macrophages, causing FIP. However, the molecular basis for this biotype switch is unknown. We examined a furin cleavage site in the region between receptor-binding (S1) and fusion (S2) domains of the spike of serotype 1 FCoV. FECV sequences were compared with FIPV sequences. All FECVs had a conserved furin cleavage motif. For FIPV, there was a correlation with the disease and >1 substitution in the S1/S2 motif. Fluorogenic peptide assays confirmed that the substitutions modulate furin cleavage. We document a functionally relevant S1/S2 mutation that arises when FIP develops in a cat. These insights into FIP pathogenesis may be useful in development of diagnostic, prevention, and treatment measures against coronaviruses.

KEYWORDS:

FECV; FIP; FIPV; Macrophage; conserved furin cleavage motif; feline coronavirus; feline enteric coronavirus; feline infectious peritonitis; feline infectious peritonitis virus; pathology; protease; protein processing; viruses

PMID:
23763835
PMCID:
PMC3713968
DOI:
10.3201/eid1907.121094
[Indexed for MEDLINE]
Free PMC Article
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