Severe seasonal influenza in ferrets correlates with reduced interferon and increased IL-6 induction

Abstract Even though ferrets are one of the principal animal models for influenza pathogenesis, the lack of suitable immunological reagents has so far limited their use in host response studies. Using recently established real-time PCR assays for a panel of ferret cytokines, we analyzed the local fe...

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Bibliographic Details
Published in:Virology (New York, N.Y.) N.Y.), 2008-06, Vol.376 (1), p.53-59
Main Authors: Svitek, Nicholas, Rudd, Penny A, Obojes, Karola, Pillet, Stéphane, von Messling, Veronika
Format: Article
Language:English
Subjects:
animal disease models
Animals
Body Temperature
Body Weight
Cytokine response
disease severity
Ferret model
Ferrets
Gene Expression Profiling
histopathology
host-pathogen relationships
human health
Human seasonal influenza strains
immune response
Infectious Disease
Influenza A
Influenza A virus
Influenza A Virus, H1N1 Subtype - growth & development
Influenza A Virus, H1N1 Subtype - immunology
Influenza A Virus, H3N2 Subtype - growth & development
Influenza A Virus, H3N2 Subtype - immunology
Innate immune response inhibition
interferons
Interferons - genetics
Interferons - immunology
interleukin-6
Interleukin-6 - genetics
Interleukin-6 - immunology
Interleukin-8 - genetics
Interleukin-8 - immunology
Lung - pathology
Lung - virology
macrophages
Male
Molecular Sequence Data
Mustela
Orthomyxoviridae Infections - immunology
Orthomyxoviridae Infections - virology
Pathogenesis
respiratory system
Seasons
Severity of Illness Index
viral diseases of animals and humans
virulence
Virus-host interactions
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Summary:Abstract Even though ferrets are one of the principal animal models for influenza pathogenesis, the lack of suitable immunological reagents has so far limited their use in host response studies. Using recently established real-time PCR assays for a panel of ferret cytokines, we analyzed the local ferret immune response to human influenza isolates of the H1N1 and H3N2 subtypes that varied in their virulence. We observed that the severity of clinical signs correlated with gross- and histopathological changes in the lungs and was subtype-independent. Strains causing a mild disease were associated with a strong and rapid innate response and upregulation of IL-8, while severe infections were characterized by a lesser induction of type I and II interferons and strong IL-6 upregulation. These findings suggest that more virulent strains may interfere more efficiently with the host response at early disease stages.
ISSN:0042-6822
1096-0341
DOI:10.1016/j.virol.2008.02.035