Back 'n' forth about evolution of virulence and avian flu

Posted 7 November 2005 by Tara Smith

There's been some interesting discussion over on SciAm Observations about the evolution of infectious diseases, and notably, influenza. It all started with editor John Rennie's post, discussing an article on H5N1 written by Wendy Orent, here: Part I Wendy Orent and evolutionary biologist Paul Ewald both replied in Part II and Part III, respectively: Part II Part III Both discussed Rennie's mention of a critique of Orent's article on the public health blog, Effect Measure. The pseudomynous Revere from that blog then replied in Part IV: Part IV (Continued at Aetiology...)

7 Comments

GT(N)T · 7 November 2005

"His theory states that high virulence should only occur in an immobilized host--such as was the condition on the western front during WWI, which he claims enabled the Spanish flu to become so virulent. I've read many of Ewald's works on this (for those of you unfamiliar with his theory, the most comprehensive discussion is in 1994's Evolution of Infectious Diseases; other writings are listed here, and a freely available Emerging Infectious Diseases article on the topic is here). I think he has some excellent ideas, but I agree with Revere (though I'd say it in a much nicer way :) ) that Ewald's claims are "too sweeping."

I think that if you looked at Ewald's 'theory' as a hypothesis, or set of hypotheses, it wouldn't seem so sweeping. They would simply be a set of statements in need of testing.

By the way, his criticism that some researchers focus on mutation and genomic alteration, ignoring natural selection, seems an apt warning.

You are working in a fascinating area of biology. Thanks for the insights and updates.

Tara Smith · 7 November 2005

I think that if you looked at Ewald's 'theory' as a hypothesis, or set of hypotheses, it wouldn't seem so sweeping. They would simply be a set of statements in need of testing.

And I could totally get on board with that, but Ewald (IMO) suggests that it's been tested more thoroughly than it has.

The track record of the past half century has shown that a severe pandemic of the 1918 virulence has not happened even though influenza experts were often saying that it was imminent. We now know that their predictions, at least for this period of time, were wrong. With regard to the future I am predicting that such a highly lethal pandemic (i.e., 1 death per 50 infections) will not occur, not from H5N1 and not from any other influenza virus that will arise unless regional conditions allow transmission from immobile hosts, as they did on the Western Front in 1918. This is not "speculation" as is claimed by our hooded critic with the self-aggrandizing name. It is a prediction based on careful consideration of theory and evidence. The future will demonstrate whether it is accurate.
— Ewald

All well and good, but what do we do in the meantime? Sit around and twiddle our thumbs while we wait for the next pandemic to see if his predictions hold? And even if they do, what does that tell us--was it a fluke, or is he really onto something? An event that occurs only a few times a century isn't the best example to validate your model. :) He also talks a lot about "gradual" this and "slow" that--all relative words that can't be easily quantitated, yet a lot of his results hinge on those descriptors. Note that he uses Ebola as one example of his theory in action. But let's take a look at this quote:

The last century represents countless thousands of "natural experiments" involving countless trillions of mutation-prone viruses. If the highly virulent variants were able to spread in competition with strains of low or moderate virulence we would see some evidence of regional outbreaks. Instead we see only epidemics and pandemics of low to moderate virulence.
— Ewald

Hmmm...highly virulent variants, possibly able to spread in competition with strains of low or moderate virulence, leading to regional outbreaks. Isn't that almost exactly what I just described in this post on Ebola evolution? Again, I don't want to come down too harshly on Ewald, because I do think many of his ideas have merit--he seems to just want to promote them as a law of nature or something (and therefore, anyone disagreeing with him is either incompetent or stupid), and I think that's a big mistake.

By the way, his criticism that some researchers focus on mutation and genomic alteration, ignoring natural selection, seems an apt warning.

Could be, but again, I really don't see it. As I mentioned, papers published in this area certainly take this into account as best as they can (the stochastic nature of the processes making it a difficult task). But granted, it's always something to keep in mind, and it likely couldn't hurt to have it a bit more on the front burner.

Michael Hopkins · 7 November 2005

So that is why the Sci Am blog has had no entries in months. They changed their location and did not bother to mention this at their old location that they were moving. And I thinking that Rennie got tired of blogging or did not have enough time.

Pierce R. Butler · 7 November 2005

According to Ewald's model, the flu of 1918 got its punch from incubating in the trenches, hospitals, and troops transports of the Western Front of WWI, where sick & healthy were forced together in large numbers: this supposedly cancelled out the self-limiting dynamics of virulent infection whereby the nastiest cases die before they can affect others.

Agreed, things got very ugly during The Great War, but - from a bug's point of view - don't conditions of crowding and helter-skelter health care in many "third world" megaslums and refugee camps (not to mention poultry factories) offer basically similar opportunities now?

morbius · 7 November 2005

Consider the immobility of New Orleans.

Tara Smith · 8 November 2005

According to Ewald's model, the flu of 1918 got its punch from incubating in the trenches, hospitals, and troops transports of the Western Front of WWI, where sick & healthy were forced together in large numbers: this supposedly cancelled out the self-limiting dynamics of virulent infection whereby the nastiest cases die before they can affect others. Agreed, things got very ugly during The Great War, but - from a bug's point of view - don't conditions of crowding and helter-skelter health care in many "third world" megaslums and refugee camps (not to mention poultry factories) offer basically similar opportunities now?
— Pierce R. Butler

He does (somewhat) address that, at least with regard to chickens:

n my 1994 book, Evolution of Infectious Disease, I added a fourth prediction, which is that we will continue to get severe influenza epidemics in chicken farms so long as the conditions in chicken farms, like the conditions at the Western Front, allow transmission from immobile chickens. This prediction has been confirmed by the lethal outbreaks of H5N1 in Asia and H5N2 in Mexico. Anyone who dismisses this analysis as speculation does not understand how the scientific process works or what scientific theory actually is, at least with regard to evolutionary biology.

I've not read anything of his that suggests he thinks the *human* conditions in those types of areas would be sufficient, though--and indeed, his response to scientists' concerns over H5N1 seem to think he disagrees that they would be enough to cause a highly lethal pandemic.

Pierce R. Butler · 10 November 2005

Ewald: ... we will continue to get severe influenza epidemics in chicken farms so long as the conditions in chicken farms, like the conditions at the Western Front, allow transmission from immobile chickens.

Maybe by "immobile" he means something like "in close contact over prolonged periods of time" - relatively few doughboys were crammed in cages, after all. This definition also seems to require large populations in such conditions, but that also remains implicit. (Ewald's idea seems as if it could be quantifiable: n vectors * n*x contacts among vectors * y initial virus variants * t time...) The post-Katrina situation in New Orleans was an invitation to major disease outbreaks, due to crowding, stress, horrible sanitation, lack of clean water & food, shortages of medical personnel & supplies, etc (we're lucky it didn't get even worse) - but I doubt that lasted long enough to become the sort of pandemic flu incubator Ewald envisions. However, to the very limited degree to which I understand his model, it surely seems applicable to, say, refugee camps in Darfur, Pakistan, & the Congo, slums in Sao Paolo, Lagos, Manila, Port-au-Prince, and all too many other overcrowded chronic hellholes around the planet.