#214
Yesterday, with the aid of information released by scientists in Japan, Britain and the United States, we now are a little closer to understanding why the H5N1 Avian Flu virus has not (as yet) gained efficient human-to-human (H2H) transmissibility, and what it may take for the virus to mutate to become a pandemic strain.
I’ll leave the heavy lifting to blogs like Effect Measure, which I’m sure will tackle the hard science of this subject in the coming days, and simply give you the 8th grade science class version, which is more my speed.
To date, the H5N1 virus is well adapted to infecting birds, but not so well adapted to infecting humans. Sure, it happens, but not very often, and rarely in a chain of infections.
Why? Well it all has to do with receptor cells.
Receptor cells are cells found deep in the lungs and in the lining of the airway passages that allow a virus to attach to, and infect the host. Think of these cells as chemical `locks’, that require a specific amino acid `key’ in the virus to open.
Bird receptor cells are chemically slightly different from human receptor cells. For those craving scientific verbiage, avian receptor cells are of the sialic a2,3 variety and human receptor cells are sialic a2,6. Aren’t you glad you asked?
Anyway.
The H5N1 virus has tiny spikes on its surface, like tiny chemical keys sticking out, and these chemical `keys’ bind to the avian a2,3 receptor cells nicely, thus making the virus the scourge of the bird kingdom, but not infecting a lot of humans. People do have a few of the avian-like a2,3 receptor cells deep in their lungs, enough to allow some infections, but not enough to permit efficient H2H transmission.
It would seem then that the H5N1 virus poses little threat to humans. And that would be true if the virus were not constantly changing, or mutating. As it mutates it picks up, or swaps, genetic material, and thus changes its genetic sequence.
Scientists have determined two areas of it’s genetic sequence where a small amino acid change, if they occur, would give the virus the ability to easily attach to human receptor cells and threaten a human pandemic.
They also admit there may be changes to other areas of the virus which might produce the same result.
Even more ominously, they also report that both amino acid changes have been observed in sequences of the H5N1 virus in the past. As for why the strain didn’t go pandemic then, they aren’t really sure. It suggests that additional changes to the virus may be needed.
Where does this leave us? Are we closer to a pandemic today than we were yesterday?
No, not really. Knowing doesn't really change anything. The virus works on its own timetable, and will do what it will do. We are simply a little further along the road of our understanding of this virus, and how it works. We now have an area of the virus to watch, to see if it is mutating in the direction of a pandemic strain, and a basis for further research.
This study may, however, help dispel the notion that there is some species barrier, some physical reason why the virus cannot evolve into a human strain.
But there are still questions unanswered.
If these changes have been observed before, and an efficient H2H strain didn’t emerge, what stopped it?
What other areas of the H5N1 virus, if changed, would also turn the virus into a pandemic threat?
And the $64,000 question, assuming it does happen, how long do we have before the virus becomes easily spread H2H?
These questions, along with a lot of others, continue to give research scientists around the world a nightly case of heartburn.
For now, all we really know is that the changes required not only are possible, they have already been observed. And that should be a real wakeup call.
As more and more hosts are infected, more permutations of the virus are generated, and the odds increase that the right combination of changes will eventually occur to produce the perfect viral storm.
As far as whether it will happen?
Stay tuned.
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