Marine mammals are a relatively under studied host for influenza viruses, although their susceptibility to influenza A infection has been known since 1981 (cite Characterization of an influenza A virus from seals Webster et al.).
While it doesn't happen often, mass mortality and morbidity events have been observed in seal populations over the years due to mostly avian influenza viruses. (note: Human H1N1pdm09 was detected in Elephant Seals in 2010).
- During the winter of 1979-1980 seals were found suffering from pneumonia on the Cape Cod. In that instance, the culprit turned out to be an H7N7 influenza. (see Isolation of an influenza A virus from seals G. Lang, A. Gagnon and J. R. Geraci)
- In 1984 influenza subtype H4N5 – a strain previously only seen in birds – was determined to be behind the deaths of a number of New England seals in 1982 and 1983 (cite Are seals frequently infected with avian influenza viruses? R G Webster et al.)
- And in 1995, in the Journal of General Virology, authors R. J. Callan, G. Early, H. Kida and V. S. Hinshaw wrote of the The appearance of H3 influenza viruses in seals during the early 1990s.
- Seals have also been shown susceptible to influenza B (cite Influenza B virus in seals. Osterhaus AD, Fouchier , et al.).
- And most recently (in 2014), as many as 3,000 European Harbor seals died due to an outbreak of H10N7 (see SwAM: European Seal Deaths Continue From H10N7 Flu).
Seals, since they sometimes consume shore birds, are at heightened risk of avian flu exposure. In 2011 we saw a mass die off of seals in New England due to avian H3N8 (see New England Seal Deaths Tied to H3N8 Flu Virus).
Until it landed in seals, this H3N8 strain was an avian adapted virus. That is, that it bound preferentially to the kind of receptor cells commonly found in the digestive and respiratory tracts of birds; alpha 2,3 receptor cells.
In 2012, in mBio: A Mammalian Adapted H3N8 In Seals, we saw evidence that that particular avian virus had recently adapted to better bind to alpha 2,6 receptor cells; the type that line the surfaces of the human upper respiratory system.
Additional research, published later that year (see Nature Comms: Respiratory Transmission of Avian H3N8 In Ferrets), confirmed that this `virus has an increased affinity for mammalian receptors, transmits via respiratory droplets in ferrets and replicates in human lung cells.’
These findings set off some alarm bells, as seals were suddenly on the radar as potential `mixing vessels’ for influenza, much in the same way as pigs have been for years.
An H3N8 virus is thought to have sparked the 1900 influenza pandemic, and is considered a prime candidate to return someday(see Are Influenza Pandemic Viruses Members Of An Exclusive Club?), so the appearance of an `avian H3N8' apparently acquiring mammalian adaptations continues to spark interest.
Fast forward to today, and we have a new report, published this past week in Nature's Science Reports, that takes a deeper look at the ability of this seal H3N8 virus to bind to the mammalian alpha 2,6 receptor cell.
The authors outline their reasons for concern in the introduction:
The wide variety of IAV strains infecting seals provides opportunities for genetic reassortment and/or adaptation, and it has been proposed that seals might play a similar role to pigs as mixing vessels for avian and human viruses. With the exponential increase in protected seal populations and urbanization of coastal cities, the seal-human interface is continuously expanding, which creates a suitable environment for viral zoonotic transmissions
In contrast to some of the earlier studies on this seal H3N8 virus, these researchers (using a recombinant seal H3N8 virus) found the virus still binds preferentially to avian alpha 2,3 receptor cells. The authors write:
We compared the binding patterns of recombinant HA proteins derived from seal H3N8 against that of a seasonal human H3N2 virus (A/Wyoming/03/2003) to fixed human lung and tracheal tissue sections. HA proteins were allowed to bind to respiratory tissues, bound HA was detected by immuno-staining and the results were verified against negative control mock-stained tissue sections.
Our results revealed that, in contrast to human H3N2, seal H3N8 HA exhibited minimal to no binding to the human trachea (Fig. 2). Nonetheless, it displayed greater binding affinity than the human H3N2 to human lung tissues.
Not quite as worrisome as earlier reports suggested, but not without some concerns. The authors write:
In conclusion, seal H3N8 virus still maintains the avian-type receptor specificity, binds to human lung tissues and replicates in human lung carcinoma cells, which raises concerns about its potential to establish infection in the lower respiratory tract of humans. However, we believe that certain additional mutations will be required for this virus to gain human transmissibility.
Follow the link below for the full study, which includes a great deal of technical detail on how they created a recombinant HA for testing.