Influenza A and B Virus Attachment to Respiratory Tract in Marine Mammals - Vol. 18 No. 5 - May 2012 - Emerging Infectious Disease journal - CDC
Volume 18, Number 5—May 2012
Influenza A and B Virus Attachment to Respiratory Tract in Marine Mammals
Suggested citation for this article
Understanding is limited about factors determining the ability of influenza viruses to cross the species barrier and persist in a new host population (1,2). In marine mammals, several subtypes of avian influenza A virus have caused epidemics in harbor seals (Phoca vitulina) (3–6). Also, human influenza B virus has been detected in harbor seals (7). These observations indicate the ability of both viruses to cross the species barrier and persist in harbor seals. In other marine mammal species, outbreaks of avian influenza A virus or infection with human influenza B virus have not been reported.
AbstractPatterns of virus attachment to the respiratory tract of 4 marine mammal species were determined for avian and human influenza viruses. Attachment of avian influenza A viruses (H4N5) and (H7N7) and human influenza B viruses to trachea and bronchi of harbor seals is consistent with reported influenza outbreaks in this species.
Attachment of influenza virus to tissues in the respiratory tract is a major determinant of host susceptibility to infection, efficiency of transmission, and pathogenicity and has been studied only to a limited degree (8,9). Attachment is determined largely by the specificity with which influenza virus attaches to sialosaccharide receptors on the host cell surface. In general, human influenza viruses prefer sialosaccharides in which sialic acid is linked to galactose by an α-2,3 linkage (SA-α-2,3-Gal), and avian influenza viruses prefer those with an α-2,6 linkage (SA-α-2,6-Gal) (10).
To understand differences in these properties between harbor seals and other marine mammals, we determined patterns of attachment for influenza virus strains known to have infected the respiratory tract of harbor seals, gray seals (Halichoerus grypus), harbor porpoises (Phocoena phocoena), and bottlenose dolphins (Tursiops truncatus). We chose gray seals, porpoises, and dolphins because their ranges overlap those of harbor seals and they are commonly kept in captivity.
We determined patterns of attachment to respiratory tract tissues of 4 sympatric marine mammal species for several influenza viruses. Avian influenza A virus subtypes H7N7 (A/Seal/Massachusetts/1/80) and H4N5 (A/Seal/Ma/47/83) were chosen because they had caused outbreaks in harbor seals (4,5). An influenza B virus strain (B/Seal/Netherlands/1/99) was chosen because it had been isolated from a harbor seal (7).
For each of these 3 viruses, we also included a closely related strain from the putative donor host species (H7N7 A/Mallard/Sweden/100/02, H4N5 A/Mallard/Netherlands/13/2008, and B/Harbin/7/94, respectively) to determine whether adaptation to the new host species was associated with a change in attachment. Influenza virus A(H1N1)pdm09 (A/Netherlands/164/09) and seasonal subtype (H3N2) virus (A/Netherlands/213/03) were chosen because they circulate endemically in humans and might have contact with captive marine mammals through their caretakers. All viruses were isolated as described (11–13).
We obtained respiratory tract specimens from marine mammals from archives of paraffin-embedded tissues. Trachea and lung (including bronchus, bronchiole, and pulmonary alveoli) from 3 animals per species were examined.
Attachment of influenza virus to tissues was visualized by histochemical analysis as described (13). A positive result by light microscopy was granular to diffuse red staining on the apical surface of epithelial cells in trachea, bronchi, and bronchioles and on alveolar cells. Staining was scored as the percentage of cells in a section showing virus attachment. We also evaluated virus attachment to submucosal glands.