Emergence of Fatal Avian Influenza in New England Harbor Seals
S. J. Anthonya,b, J. A. St. Legerc, K. Pugliaresd, H. S. Ipe, J. M. Chanf, Z. W. Carpenterf, I. Navarrete-Maciasa, M. Sanchez-Leona, J. T. Salikig, J. Pedersenh, W. Kareshb, P. Daszakb, R. Rabadanf, T. Rowlesi, and W. I. Lipkina
+ Author Affiliations
Center for Infection and Immunity, Mailman School of Public Health, Columbia University, New York, New York, USAa;
EcoHealth Alliance, New York, New York, USAb;
SeaWorld, San Diego, California, USAc;
New England Aquarium, Boston, Massachusetts, USAd;
National Wildlife Health Center, United States Geological Survey, Madison, Wisconsin, USAe;
Center for Computational Biology and Bioinformatics, Department of Biomedical Informatics, Columbia University, New York, New York, USAf;
Athens Veterinary Diagnostic Laboratory, University of Georgia, Athens, Georgia, USAg;
National Veterinary Services Laboratory, United States Department of Agriculture, Washington, DC, USAh; and
National Oceanic and Atmospheric Administration, Washington, DC, USAi
Address correspondence to S. J. Anthony,
sja2127@columbia.edu, or W. I. Lipkin,
wil2001@columbia.edu; for questions on computational modeling, contact R. Rabadan,
rabadan@dbmi.columbia.edu.
Editor Anne Moscona, Weill Medical College, Cornell University
ABSTRACT
From September to December 2011, 162 New England harbor seals died in an outbreak of pneumonia. Sequence analysis of postmortem samples revealed the presence of an avian H3N8 influenza A virus, similar to a virus circulating in North American waterfowl since at least 2002 but with mutations that indicate recent adaption to mammalian hosts. These include a D701N mutation in the viral PB2 protein, previously reported in highly pathogenic H5N1 avian influenza viruses infecting people. Lectin staining and agglutination assays indicated the presence of the avian-preferred SAα-2,3 and mammalian SAα-2,6 receptors in seal respiratory tract, and the ability of the virus to agglutinate erythrocytes bearing either the SAα-2,3 or the SAα-2,6 receptor. The emergence of this A/harbor seal/Massachusetts/1/2011 virus may herald the appearance of an H3N8 influenza clade with potential for persistence and cross-species transmission.
IMPORTANCE The emergence of new strains of influenza virus is always of great public concern, especially when the infection of a new mammalian host has the potential to result in a widespread outbreak of disease. Here we report the emergence of an avian influenza virus (H3N8) in New England harbor seals which caused an outbreak of pneumonia and contributed to a U.S. federally recognized unusual mortality event (UME). This outbreak is particularly significant, not only because of the disease it caused in seals but also because the virus has naturally acquired mutations that are known to increase transmissibility and virulence in mammals. Monitoring the spillover and adaptation of avian viruses in mammalian species is critically important if we are to understand the factors that lead to both epizootic and zoonotic emergence.
Footnotes
S.J.A. and J.A.S.L. contributed equally to the study.
T.R. and W.I.L. are joint senior authors.
Citation Anthony SJ, et al. 2012. Emergence of fatal avian influenza in New England harbor seals. mBio 3(4):e00166-12. doi:10.1128/mBio.00166-12.
Received 31 May 2012 Accepted 29 June 2012 Published 31 July 2012
http://mbio.asm.org/content/3/4/e00166-12
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