Spike protein fusion peptide and feline coronavirus virulence

Coronaviruses are well known for their potential to change their host or tissue tropism, resulting in unpredictable new diseases and changes in pathogenicity; severe acute respiratory syndrome and feline coronaviruses, respectively, are the most recognized examples. Feline coronaviruses occur as 2 p...

Full description

Saved in:
Bibliographic Details
Published in:Emerging infectious diseases 2012-07, Vol.18 (7), p.1089-1095
Main Authors: Chang, Hui-Wen, Egberink, Herman F, Halpin, Rebecca, Spiro, David J, Rottier, Peter J M
Format: Article
Language:English
Subjects:
Amino Acid Sequence
Animals
Base Sequence
Cats
Coronavirus Infections - virology
Coronavirus, Feline - genetics
Coronavirus, Feline - metabolism
Coronavirus, Feline - pathogenicity
Coronaviruses
feline coronavirus
Feline Infectious Peritonitis - virology
feline infectious peritonitis virus
Genetic aspects
Genome, Viral
Membrane Glycoproteins - genetics
Membrane Glycoproteins - metabolism
Molecular Sequence Data
Mutation
pathogenesis
Peptides - genetics
Recombinant Fusion Proteins - genetics
Sequence Alignment
Sequence Analysis, DNA
Spike Glycoprotein, Coronavirus
Veterinary epidemiology
Viral Envelope Proteins - genetics
Viral Envelope Proteins - metabolism
virulence
Virulence (Microbiology)
Virulence - genetics
Virus research
virus tropism
zoonoses
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Coronaviruses are well known for their potential to change their host or tissue tropism, resulting in unpredictable new diseases and changes in pathogenicity; severe acute respiratory syndrome and feline coronaviruses, respectively, are the most recognized examples. Feline coronaviruses occur as 2 pathotypes: nonvirulent feline enteric coronaviruses (FECVs), which replicate in intestinal epithelium cells, and lethal feline infectious peritonitis viruses (FIPVs), which replicate in macrophages. Evidence indicates that FIPV originates from FECV by mutation, but consistent distinguishing differences have not been established. We sequenced the full genome of 11 viruses of each pathotype and then focused on the single most distinctive site by additionally sequencing hundreds of viruses in that region. As a result, we identified 2 alternative amino acid differences in the putative fusion peptide of the spike protein that together distinguish FIPV from FECV in >95% of cases. By these and perhaps other mutations, the virus apparently acquires its macrophage tropism and spreads systemically.
ISSN:1080-6040
1080-6059
DOI:10.3201/eid1807.120143