Emergence of fatal avian influenza in New England harbor seals.

S J Anthony1 J A St Leger K Pugliares H S Ip J M Chan Z W Carpenter I Navarrete-Macias M Sanchez-Leon J T Saliki J Pedersen W Karesh P Daszak R Rabadan T Rowles W I Lipkin
Affiliations 1 institutions
  1. Center for Infection and Immunity, Mailman School of Public Health, Columbia University, New York, NY, USA. [email protected]

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. 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.

Supporting text Virus Host Location
Animals 1948 Communicable Diseases, Emerging 33 Disease Outbreaks 170 Humans 1440 Influenza A Virus, H3N8 Subtype 13 Influenza A Virus, H5N1 Subtype 300 Influenza, Human 286 Molecular Sequence Data 160 Mutation 209 New England 5 Orthomyxoviridae Infections 228 Phoca 2 Phylogeny 805 Pneumonia 3 Viral Proteins 152 Virulence 108

Evidence records

4 total
Zoonotic Surveillance
1 records · 1 evidence types
Evidence type
1 records
OVE1251
Key finding

Avian H3N8 influenza A virus was detected in postmortem samples from New England harbor seals during a pneumonia outbreak.

Virus
Host
Location
Supporting text

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.

Method
sequence analysis
Sample type
postmortem samples
Geographic raw
New England
Country inferred
USA
Transmission Evidence
1 records · 1 evidence types
Evidence type
1 records
OVE1254
Key finding

An avian influenza virus (H3N8) was transmitted from birds to New England harbor seals, causing an outbreak of pneumonia.

Virus
Host
Location
Supporting text

Here we report the emergence of an avian influenza virus (H3N8) in New England harbor seals which caused an outbreak of pneumonia.

Method
sequence analysis | postmortem sampling
Study design
field outbreak investigation with sequence analysis
Transmission direction
animal-to-animal
Geographic raw
New England
Functional Mechanism
2 records · 2 evidence types
Evidence type
1 records
OVE1253
Key finding

Avian H3N8 influenza A virus from harbor seals bound both avian-type SAα-2,3 and mammalian-type SAα-2,6 sialic acid receptors, indicating dual receptor usage.

Virus
Host
Location
Not specified
Supporting text

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.

Method
lectin staining | agglutination assay
Receptors
SAα-2,3 | SAα-2,6
Evidence type
1 records
OVE1252
Key finding

The avian H3N8 influenza A virus detected in New England harbor seals carries a PB2 D701N mutation associated with adaptation to mammalian hosts.

Virus
Host
Not specified
Location
Not specified
Supporting text

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.

Genes or proteins
PB2
Mutations
D701N
Mechanism types
host-range expansion