Seals in New England having been dying of a new type of intermediary flu. It turns out that seals are susceptible to both avian and mammal flues, which makes them a sort mixing vessel repository for both types. This new type type of flue, H3N8, is thought to have come from birds, but seals of course are not birds... and thus the term intermediary.
The discovery highlights the concern that potentially pandemic influenza can come from very unexpected sources.
Matt McGrath, BBC News, 31 July 2012 (hat tip: NC)
Researchers were puzzled by the mysterious deaths from pneumonia of 162 harbour seals around the coast of New England last year.
Autopsies on five of the marine mammals indicate that they died from a type of H3N8 influenza A virus that is closely related to a strain circulating in North American birds since 2002.
Another report added details:
Columbia University Mailman School Press Release via Medical Express
Based on full genome sequencing and phylogenetic analysis, seal H3N8 descended from an avian strain that has been circulating in North American waterfowl since 2002, which implies recent transmission from wild birds to seals.
Accordingly, seal H3N8 has acquired the ability to bind sialic acid receptors that are commonly found in the mammalian respiratory tract. Mutations in the HA and PB2 genes - required for cell entry and replication, respectively - suggest enhanced virulence and transmission in mammals, but these putative attributes require further investigation. Given these findings along with the long history of the spread of avian influenza to humans-most notably H1N1 and H5N1-seal H3N8 could pose a threat to public health.
The report is published at mBio here (ll pages), and rather publicly minded, is not gated.
Emergence of Fatal Avian Influenza in new England Harbor Seals
Anthony, et al, mBio, 31 July 2012
The seal H3N8 genome was interrogated for any genetic features that might contribute to enhanced transmissibility and virulence in seals. Expression of a second peptide (PB1-F2) from segment 2 has been associated with an increase in pathogenicity by inducing apoptosis and increasing both inflammation and secondary bacterial pneumonia (9, 10). The seal H3N8 virus contains an intact open reading frame for the pathogenic version of this accessory protein, which includes a serine at amino acid position 66 (9). All five seals had evidence of apoptosis and secondary bacterial pneumonia.
Glycosylation can also affect pathogenicity in influenza viruses (11-14). Six potential glycosylation sites were detected in the seal H3N8 HA, based on the sequence X_2X_1NX(S/T) X+1, at amino acid positions 24, 38, 54, 181, 301, and 499. None had features suggestive of inactivity or reduced efficiency, as was previously demonstrated for H5N2 (12). Many H5N1 viruses have an additional glycosylation site at positions 158 to 160, and previous work demonstrated that the deletion of this site is critical for H5N1viruses to bind to human-SA 2,6-like receptors and to transmit between mammals (15). This glycosylation site is missing in the seal H3N8 HA....
It continues on, but best as I can tell, the results are not encouraging, which is not surprising in a virus that is killing mammals.
I wasn't trying to become the sniffles, colds, coughs, and flu blog, but there just seems to be a lot of "interesting" news of late. Likely because pandemic disease is one of the potentially existential risks that our society, and thus our media, is willing to take seriously.
|Lung damage to the seals (from page 2, see mBio link above)|