Giuseppe
Emeritus
J Virol. 2009 Feb 4. [Epub ahead of print]
Intranasal Administration of Interferon-Alpha Reduces Seasonal Influenza A Virus Morbidity in Ferrets.
Kugel D, Kochs G, Obojes K, Roth J, Kobinger GP, Kobasa D, Haller O, Staeheli P, von Messling V. - Department of Virology, University of Freiburg, Germany; Institute for Veterinary Physiology, University of Giessen, Germany; Special Pathogens Program, Respiratory Viruses Program, National Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, Canada; Department of Medical Microbiology, University of Manitoba, Winnipeg, Canada; INRS-Institut Armand-Frappier, University of Quebec, Montreal, Canada.
The type I interferon (IFN) response represents one of the first lines of defense against influenza virus infections.
In this study we assessed the protective potential of exogenous IFN-alpha against seasonal and highly pathogenic influenza viruses in ferrets.
Intranasal treatment with IFN-alpha several hours before infection with the H1N1 influenza A virus strain USSR/90/77 reduced viral titers in nasal washes at least 100-fold compared to mock-treated controls.
IFN-treated animals developed only mild and transient respiratory symptoms, and the characteristic fever peak seen in mock-treated ferrets two days after infection was not observed.
Repeated application of IFN-alpha substantially increased the protective effect of the cytokine treatment.
IFN-alpha did not increase survival after infection with the highly pathogenic H5N1 avian influenza A virus strain Vietnam/1203/2004.
However, viral titers in nasal washes were significantly reduced at days one and three post infection.
Our study shows that intranasal application of IFN-alpha can protect ferrets from seasonal influenza viruses, which replicate mainly in the upper respiratory tract, but not from highly pathogenic influenza viruses, which also disseminate to the lung.
Based on these results, a more intensive evaluation of IFN-alpha as an emergency drug against pandemic influenza A is warranted.
PMID: 19193792 [PubMed - as supplied by publisher]
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Intranasal Administration of Interferon-Alpha Reduces Seasonal Influenza A Virus Morbidity in Ferrets.
Kugel D, Kochs G, Obojes K, Roth J, Kobinger GP, Kobasa D, Haller O, Staeheli P, von Messling V. - Department of Virology, University of Freiburg, Germany; Institute for Veterinary Physiology, University of Giessen, Germany; Special Pathogens Program, Respiratory Viruses Program, National Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, Canada; Department of Medical Microbiology, University of Manitoba, Winnipeg, Canada; INRS-Institut Armand-Frappier, University of Quebec, Montreal, Canada.
The type I interferon (IFN) response represents one of the first lines of defense against influenza virus infections.
In this study we assessed the protective potential of exogenous IFN-alpha against seasonal and highly pathogenic influenza viruses in ferrets.
Intranasal treatment with IFN-alpha several hours before infection with the H1N1 influenza A virus strain USSR/90/77 reduced viral titers in nasal washes at least 100-fold compared to mock-treated controls.
IFN-treated animals developed only mild and transient respiratory symptoms, and the characteristic fever peak seen in mock-treated ferrets two days after infection was not observed.
Repeated application of IFN-alpha substantially increased the protective effect of the cytokine treatment.
IFN-alpha did not increase survival after infection with the highly pathogenic H5N1 avian influenza A virus strain Vietnam/1203/2004.
However, viral titers in nasal washes were significantly reduced at days one and three post infection.
Our study shows that intranasal application of IFN-alpha can protect ferrets from seasonal influenza viruses, which replicate mainly in the upper respiratory tract, but not from highly pathogenic influenza viruses, which also disseminate to the lung.
Based on these results, a more intensive evaluation of IFN-alpha as an emergency drug against pandemic influenza A is warranted.
PMID: 19193792 [PubMed - as supplied by publisher]
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