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Published Online July 2, 2009
Science DOI: 10.1126/science.1177127

Reports

Submitted on June 1, 2009
Accepted on June 23, 2009

Pathogenesis and Transmission of Swine-Origin 2009 A(H1N1) Influenza Virus in Ferrets

Vincent J. Munster 1{dagger}, Emmie de Wit 1{dagger}, Judith M. A. van den Brand 1, Sander Herfst 1, Eefje J. A. Schrauwen 1, Theo M. Bestebroer 1, David van de Vijver 1, Charles A. Boucher 1, Marion Koopmans 2, Guus F. Rimmelzwaan 1, Thijs Kuiken 1, Albert D. M. E. Osterhaus 1, Ron. A. M. Fouchier 1*

1 National Influenza Center and Department of Virology, Erasmus Medical Center, Rotterdam, the Netherlands.
2 National Influenza Center and Department of Virology, Erasmus Medical Center, Rotterdam, the Netherlands.; National Institute for Public Health and the Environment, Bilthoven, the Netherlands.

* To whom correspondence should be addressed.
Ron. A. M. Fouchier , E-mail: r.fouchier{at}erasmusmc.nl

{dagger}These authors contributed equally to this work.

The swine-origin influenza A(H1N1) virus that has emerged in humans in early 2009 has raised concerns about pandemic developments. In a ferret pathogenesis and transmission model, the 2009 A(H1N1) virus was found to be more pathogenic than a seasonal A(H1N1) virus, with more extensive virus replication occurring in the respiratory tract. Replication of seasonal A(H1N1) virus was confined to the nasal cavity of ferrets, but 2009 A(H1N1) also replicated in the trachea, bronchi, and bronchioles. Virus shedding was more abundant from the upper respiratory tract for 2009 A(H1N1) virus by comparison with seasonal virus, and transmission via aerosol or respiratory droplets was equally efficient. These data suggest that the 2009 A(H1N1) virus has the ability to persist in the human population, potentially with more severe clinical consequences.


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