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Commentary

Seal H3N8 PB2 Recombination With Canine & Equine Sequences
Recombinomics Commentary 23:00
July 31, 2012

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.

The above comments are in the “significance" summary of the newly published mBio paper, “Emergence of Fatal Avian Influenza in New England Harbor Seals” by researchers at Columbia University.  The paper describes sequences from five H3N8 sets of sequences from seals who died in late 2011 off the New England coast.  The “naturally acquired mutation” of greatest concern was D701N in PB2, which is an acquisition which is known to increase avian influenza transmission in mammalian hosts.

The released PB2 sequence from a September, 2011 sample, A/harbor seal/Massachusetts/1/2011, like all five PB2 sequences, has D701N due to G2101A.  However, this change and the downstream sequence is an exact match with H3N8 PB2 sequences which are common in canine and equine isolates (see GISAID list here).

Moreover, in addition to G2101A, the PB2 sequence has acquired a cluster of three silent changes (C768T, C774T, G777A), which would have less selection pressure, yet all three changes are in a similar set of canine and equine H3N8 sequences (see list here).

The acquisition of these mammalian polymorphisms on an avian genetic background signal rapid evolution of the avian sequences toward mammalian transmission, and raise concerns of unknown hosts serving as mixing vessels for recombination and rapid influenza evolution.

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