#1221
Roughly 1 year and 1000 blogs ago I presented a slightly different version of this essay. Since it is a quiet Sunday morning, and this piece predates when my blog was `discovered' by many readers, I present it again, slightly updated.
It seems that every time we turn around, we learn something new about the H5N1 virus, and that our earlier assumptions as to how a pandemic might play out may not be valid.
Case in point: About a year ago it was announced that the expected drop in the CFR (Case Fatality Ratio) of the virus might not happen. While still speculative, for the first time some scientists are publicly considering the possibility of a mortality rate many times higher than the 1918 Spanish Flu.
Why, you might ask, are we just coming to this realization?
Well, simply put, we’ve been relying on the one major pandemic in modern history, and one lineage of influenza viruses, to base our assumptions on.
And extrapolating the future from a dataset of 1 is always dangerous.
All of our knowledge of influenzas in humans is based on the H1N1 virus and its descendents. Prior to its emergence in 1918, we honestly don’t know what flu viruses were circulating; we simply didn’t have the technology back then to determine that. In fact, it wasn’t until more than a dozen years after the end of the Spanish flu that we realized it had been caused by a virus, not a bacteria.
A smattering of history and science follows. Relax; I’ll keep it simple.
The influenza virus has 8 RNA segments: HA, NA, NP, M, NS, PA, PB1, and PB2. The virus is identified by its HA (Hemagglutinin) and NA (neuraminidase) segments.
The H1N1 virus, which caused the Spanish Flu, emerged from out of the blue and replaced all existing flu viruses in circulation. Along the way, it claimed between 20 and 50 million lives.
The Spanish flu was so deadly because it appears that it was a novel bird flu virus, and did not reassort with an existing virus to which mankind already had resistance. Much like the H5N1 virus of today.
Between 1918 and 1957, the only strain in circulation was the H1N1 or its offspring. The Asian Flu of 1957 saw that virus reassort with an unknown avian strain and acquire a new HA, NA, and PB1 protein, and it became H2N2. The other 5 gene segments remained basically the same as with the H1N1 virus.
This resulted in the Asian Flu sweeping the globe, albeit with a much lower mortality rate than 1918. The difference? Well, likely it was due to the fact that this new virus contained much of the same genetic material (5 of 8 segments) that the old Spanish flu contained, and that had been in circulation nearly 40 years by that time.
Most people had some built in immunity.
Then in 1968 (the Hong Kong Flu), the HA and PB1 got swapped for new ones again, resulting in the H3N2 virus. Five other genes were still descendants of the 1918 virus, while one was acquired in 1957.
This Hong Kong Flu, again carrying much of the genetic code from the 1918 virus, was milder still. It was a variation on an old theme, one that our immune systems had seen before.
So every ‘human’ influenza virus that we have seen in the 20th century comes from a common ancestor, the H1N1 virus. And we naturally assume that any new influenza virus that comes down the pike will act in much the same manner as what we have observed in the past.
And perhaps it will.
But to date, the H5N1 virus has shown remarkable differences from what we’ve observed before. And that is worrisome.
The lethality of this virus is far and away greater than anything we’ve ever seen in an influenza virus in the past. It appears, at least some of the time, to spread beyond the lungs and attack multiple organs: something we didn’t expect. And it appears to have caused hemorrhagic symptoms in some patients, and it may even be transmitted via body fluids, such as blood and feces.
How this virus will ultimately behave appears to depend on how it acquires the ability to be efficiently transmitted (assuming of course, that it does).
If it picks up some gene segments from another influenza virus, one that we already have been exposed to, it will likely lose some of its lethality. If, however, it simply mutates into an easily transmissible strain, and retains its novel genetic sequences, then it could be a much more formidable pathogen.
We also make assumptions on how a pandemic might play out based on how things evolved in the 1918 Spanish Flu. There, we saw multiple waves over 18 months. The waves lasted in each community for 6 to 12 weeks, and were followed by a period of low occurrence for several months.
The assumption is that we would see this same pattern. But once again, we are making assumptions based on a dataset of 1. Much has changed in the 88 years since the last pandemic. We travel far more frequently, and faster, than we did back then. Instead of taking weeks to travel around the world, we can do it in a couple of days. And if we can do it, so can a virus.
There are simply too many unknowns right now to state with certainty how things will play out in the next pandemic.
The bottom line is, despite our advancements in science and medicine over the past 88 years . . .
. . . we know less than we think we do about what the next pandemic may look like.
