Credit NIAID
# 7598
This week we’ve seen further evidence that nature’s laboratory is open 24/7, and that when it comes to viral evolution, nature is never really satisfied with the status quo.
We learned on Wednesday (see Nature: Genesis Of The H7N9 Virus) that while our attentions were focused on the H7N9 virus that infected 130+ people in China last spring, another H7 virus – H7N7 – developed in parallel with it and spread quietly among poultry.
Early experiments suggest this H7N7 virus can infect ferrets, and might have the ability jump species as has H7N9.
Also this week, the CDC’s EID journal published a paper on the H9N2 virus (which is widespread in Asian poultry and contributed genes to the emergent H7N9 and H7N7 viruses in China), looking at its genetic evolution in recent years.
Not surprisingly, they too found signs that it may be better adapting to mammals.
Antigenic and Molecular Characterization of Avian Influenza A(H9N2) Viruses, Bangladesh
Abstract
Human infection with avian influenza A(H9N2) virus was identified in Bangladesh in 2011. Surveillance for influenza viruses in apparently healthy poultry in live-bird markets in Bangladesh during 2008–2011 showed that subtype H9N2 viruses are isolated year-round, whereas highly pathogenic subtype H5N1 viruses are co-isolated with subtype H9N2 primarily during the winter months. Phylogenetic analysis of the subtype H9N2 viruses showed that they are reassortants possessing 3 gene segments related to subtype H7N3; the remaining gene segments were from the subtype H9N2 G1 clade. We detected no reassortment with subtype H5N1 viruses.
Serologic analyses of subtype H9N2 viruses from chickens revealed antigenic conservation, whereas analyses of viruses from quail showed antigenic drift. Molecular analysis showed that multiple mammalian-specific mutations have become fixed in the subtype H9N2 viruses, including changes in the hemagglutinin, matrix, and polymerase proteins.
Our results indicate that these viruses could mutate to be transmissible from birds to mammals, including humans.
It was just over 5 years ago when researchers warned that H7 viruses were becoming better adapted to human hosts (see Contemporary North American influenza H7 viruses possess human receptor specificity: Implications for virus transmissibility).
And out of left field, last year in mBio: A Mammalian Adapted H3N8 In Seals, we looked at an avian H3N8 virus – never before seen in mammals – had infected and killed harbor seals in New England.
This report found that unlike the H3N8 strain found in birds, this virus had acquired important mammalian adaptations including the ability to bind to alpha-2,6 receptor cells.
Regular readers of this blog are aware that avian influenza strains bind preferentially to the kind of receptor cells commonly found in the digestive and respiratory tracts of birds; alpha 2,3 receptor cells.
Human (and mammalian adapted) influenzas – on the other hand - bind to the kind of receptor cells that line the surfaces of the human upper respiratory system; alpha 2,6 receptor cells.
A press release from Columbia University's Mailman School of Public Health, titled An avian flu that jumps from birds to mammals is killing New England's baby seals cautioned:
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.
With H5N1, H7N9, and MERS-CoV at the forefront, and H9N2, H7N7, H3N2v, H3N8 (and many others) in the wings, it becomes a numbers game.
Millions of hosts (primarily avian and porcine), generating hundreds of trillions of viral copies every day, some percentage of which invariably carry mutations.
By far, the vast majority of these are evolutionary failures, but every so often, a more `biologically fit’ virus will emerge.
And very rarely, we’ll see one that has the ability to not only infect humans, but can out-spread and out-replicate its competitors.
That’s what happened with H1N1 in 2009, and it is what will undoubtedly happen again someday in the future as these viruses evolve and spread.
While no one can predict when or from what direction the next pandemic will come, the number of perceived threats and the level of concern in scientific circles has grown considerably over the past year.
All of which ought to make pandemic planning an important part of your overall disaster planning and preparedness effort, alongside readiness for earthquakes, hurricanes, and floods.
Accordingly, next month, during National Preparedness Month, we’ll be looking at how your pandemic plans should be evolving, to hopefully give you, your family, and your community a Darwinian advantage over the next pandemic virus that comes down the pike.
