Virulent systemic feline calicivirus infection

Local cytokine modulation and contribution of viral mutants

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

Virulent systemic feline calicivirus (VS-FCV) is a novel, emerging pathogen with mortality up to 67% even in previously healthy adult cats; VS-FCV has resulted in at least six epidemics since 1998. Affected cats have systemic vascular compromise and hemorrhagic-fever like signs in part due to viral invasion of epithelium and endothelium, coupled with host cytokine responses. Affected skin tissues had, on average, 3.8 elevated cytokines compared with control tissue, with prominent upregulation in IL-10, TNF-α, and MIP-1α. Sequencing of most of the genomes of two VS-FCV strains documented patterns of virus relatedness and implicated changes in the capsid gene in the emerging phenotype, possibly through initiation of immune mechanisms manifest in the cytokine changes. Understanding the features contributing to the emergence of this disease is critical for management and prevention of this and similar outbreaks attributable to RNA viruses in animals and humans.

Original languageEnglish (US)
Pages (from-to)55-61
Number of pages7
JournalJournal of Feline Medicine and Surgery
Volume8
Issue number1
DOIs
StatePublished - Feb 2006

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Caliciviridae Infections
Feline Calicivirus
Feline calicivirus
cytokines
Cytokines
mutants
Cats
infection
cats
capsid
Capsid
RNA Viruses
interleukin-10
endothelium
blood vessels
skin (animal)
Interleukin-10
fever
Endothelium
Disease Outbreaks

ASJC Scopus subject areas

  • veterinary(all)

Cite this

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title = "Virulent systemic feline calicivirus infection: Local cytokine modulation and contribution of viral mutants",
abstract = "Virulent systemic feline calicivirus (VS-FCV) is a novel, emerging pathogen with mortality up to 67{\%} even in previously healthy adult cats; VS-FCV has resulted in at least six epidemics since 1998. Affected cats have systemic vascular compromise and hemorrhagic-fever like signs in part due to viral invasion of epithelium and endothelium, coupled with host cytokine responses. Affected skin tissues had, on average, 3.8 elevated cytokines compared with control tissue, with prominent upregulation in IL-10, TNF-α, and MIP-1α. Sequencing of most of the genomes of two VS-FCV strains documented patterns of virus relatedness and implicated changes in the capsid gene in the emerging phenotype, possibly through initiation of immune mechanisms manifest in the cytokine changes. Understanding the features contributing to the emergence of this disease is critical for management and prevention of this and similar outbreaks attributable to RNA viruses in animals and humans.",
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AU - Pesavento, Patricia

AU - Poland, Amy

AU - Pedersen, Niels C

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