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Originally published in Science Express on 2 July 2009
Science 24 July 2009:
Vol. 325. no. 5939, pp. 484 - 487
DOI: 10.1126/science.1177238
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Reports

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

Taronna R. Maines,1 Akila Jayaraman,2 Jessica A. Belser,1 Debra A. Wadford,1 Claudia Pappas,1 Hui Zeng,1 Kortney M. Gustin,1 Melissa B. Pearce,1 Karthik Viswanathan,2 Zachary H. Shriver,2 Rahul Raman,2 Nancy J. Cox,1 Ram Sasisekharan,2 Jacqueline M. Katz,1 Terrence M. Tumpey1,*

Recent reports of mild to severe influenza-like illness in humans caused by a novel swine-origin 2009 A(H1N1) influenza virus underscore the need to better understand the pathogenesis and transmission of these viruses in mammals. In this study, selected 2009 A(H1N1) influenza isolates were assessed for their ability to cause disease in mice and ferrets and compared with a contemporary seasonal H1N1 virus for their ability to transmit to naïve ferrets through respiratory droplets. In contrast to seasonal influenza H1N1 virus, 2009 A(H1N1) influenza viruses caused increased morbidity, replicated to higher titers in lung tissue, and were recovered from the intestinal tract of intranasally inoculated ferrets. The 2009 A(H1N1) influenza viruses exhibited less efficient respiratory droplet transmission in ferrets in comparison with the highly transmissible phenotype of a seasonal H1N1 virus. Transmission of the 2009 A(H1N1) influenza viruses was further corroborated by characterizing the binding specificity of the viral hemagglutinin to the sialylated glycan receptors (in the human host) by use of dose-dependent direct receptor-binding and human lung tissue–binding assays.

1 Influenza Division, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30333, USA.
2 Harvard–Massachusetts Institute of Technology (MIT) Division of Health Sciences and Technology and Koch Institute for Integrative Cancer Research, Department of Biological Engineering, MIT, E25-519, Cambridge, MA 02139, USA.

* To whom correspondence should be addressed. E-mail: tft9{at}cdc.gov

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