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Literature detail

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]
PMID 22851656 2012 mBio eng epublish
PubMed DOI Browse context

Article

Publication summary

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.

Animals Communicable Diseases, Emerging Disease Outbreaks Humans Influenza A Virus, H3N8 Subtype Influenza A Virus, H5N1 Subtype Influenza, Human Molecular Sequence Data Mutation New England Orthomyxoviridae Infections Phoca Phylogeny Pneumonia Viral Proteins Virulence

Structured evidence records

Evidence records

6 total
Receptor Usage 2 records
Receptor Usage Extraction confidence 0.90
Key finding

The avian H3N8 influenza virus from harbor seals binds both SAα-2,3 and SAα-2,6 receptors, showing compatibility with avian and mammalian-type sialic acid receptors.

Virus
IAV H3N8
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 sialic acid receptor
Receptor Usage Extraction confidence 0.90
Key finding

The avian H3N8 influenza virus from harbor seals binds the mammalian-type SAα-2,6 sialic acid receptor, indicating adaptation to mammalian receptor usage.

Virus
IAV H3N8
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-2,6 sialic acid receptor
Cross Species Transmission 1 records
Cross Species Transmission Extraction confidence 0.90
Key finding

An avian H3N8 influenza virus circulating in North American waterfowl crossed species to infect harbor seals in New England.

Virus
IAV H3N8
Location
United States New England, United States
Supporting text

Sequence analysis 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 adaptation to mammalian hosts. Here we report the emergence of an avian influenza virus (H3N8) in New England harbor seals.

Method
sequence analysis
Study design
outbreak investigation
Transmission direction
animal-to-animal
Geographic raw
New England
Country inferred
United States
Genomic Evolution 1 records
Genomic Evolution Extraction confidence 0.80
Key finding

Genomic sequencing demonstrated an avian-origin H3N8 influenza A virus in harbor seals with a PB2 D701N mutation indicative of adaptation to mammalian hosts.

Virus
IAV H3N8
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.

Genes or proteins
PB2
Analysis methods
sequence analysis; phylogenetic analysis
Molecular Adaptation 1 records
Molecular Adaptation Extraction confidence 0.95
Key finding

The avian H3N8 influenza A virus from harbor seals possessed a PB2 D701N mutation linked to mammalian adaptation and could bind both avian and mammalian sialic acid receptors, indicating enhanced host adaptation potential.

Virus
IAV H3N8
Host
Not specified
Location
Not specified
Supporting text

Sequence analysis of postmortem samples revealed the presence of an avian H3N8 influenza A virus ... with mutations that indicate recent adaption to mammalian hosts. These include a D701N mutation in the viral PB2 protein ... 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 receptor.

Genes or proteins
PB2
Receptors
SAα-2,3; SAα-2,6
Mutations
D701N
Mechanism types
polymerase_activity; receptor_binding; host_adaptation; pathogenicity
Outbreak Investigation 1 records
Outbreak Investigation Extraction confidence 0.95
Key finding

An outbreak of pneumonia in New England harbor seals was caused by avian H3N8 influenza A virus, resulting in 162 deaths and recognized as an unusual mortality event.

Virus
IAV H3N8
Location
United States New England, United States
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. 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).

Method
Sequence analysis of postmortem samples
Transmission direction
animal-to-animal
Geographic raw
New England
Country inferred
United States
Outbreak time
September to December 2011
Outbreak scale
162 deaths