Evolution Favors New Epidemic Diseases of Intermediate Severity

This came across my feed today. https://scitechdaily.com/evolution-favors-new-epidemic-diseases-of-intermediate-severity/

I was wondering what you all thought and whether it supports, undermines or is neutral as it relates to Genetic Entropy, so I can keep that in mind as I read the book.

“For a long time, conventional wisdom held that new diseases evolved to become harmless,” said Dr. Camille Bonneaud, of the Centre for Ecology and Conservation on Exeter’s Penryn Campus in Cornwall.

“Although theoretical developments in evolutionary biology in the 1980s showed that this was not necessarily the case, such belief still holds firm, even today.

It did? It does?


We found a positive linear relationship between pathogen virulence and transmission rate to an uninfected sentinel, supporting the core assumption of the trade‐off hypothesis.

This article reminded me of this conversation. SFT: On Genetic Entropy - #800
@RonSewell do you think this affects your statement I’ve linked? Perhaps you will argue this research only relates to fitness of the pathogen in novel host species.

Sanford wants to establish virulence as a proxy for fitness, because his next step is to equate fitness with genetic perfection - that disease is directly created as Olympic gold medalist physical prowess, platonic archetype, psychopathic little killing machines. From this lofty summit, the only direction is down, and the attenuation of virulence represents loss of fitness in some sort of athletic sense.

Anything that impacts the reproduction of any organism is an input factor for fitness, including genetic makeup, but Sanford’s insistence that virulence is a proxy for fitness is simplistic and does not generalize.

If you take a camel and drop in the deep ocean, how likely is it to pass on its genes? How likely is a whale to reproduce in the middle of the Sahara? Is a creature more fit if larger or smaller, lighter or darker, cooperative or competitive? The answer to all these questions is contextual to environment, and the integration of the myriad of factors funnels down to one metric which captures it all - reproductive success. Failure leads to extinction. By definition, all our ancestors back to the beginning of life, without exception, were fit in this one regard; each of them managed to procreate.

Now relate this to smallpox. In the old world, pox came with the long association with dairy and was familiar - as the population was not immunologically naïve, although serious and potentially deadly, smallpox did not present in virulent, population threatening epidemics. In the environment of the new world, smallpox was a lethal angel of death which decimated first nations settlements. The difference in virulence was due to the host population, not the virus itself. The environmental context must be considered. While this has implications for viral reproduction, the fitness of an infectious agent is far more complex than just virulence, and what is in the interest of the pathogen shifts over time.

The paper you linked lines up with conventional understanding and I have no argument with it. Bold mine…

The virulence‐transmission trade‐off hypothesis has provided a dominant theoretical basis for predicting pathogen virulence evolution, but empirical tests are rare, particularly at pathogen emergence. The central prediction of this hypothesis is that pathogen fitness is maximized at intermediate virulence due to a trade‐off between infection duration and transmission rate. However, obtaining sufficient numbers of pathogen isolates of contrasting virulence to test the shape of relationships between key pathogen traits, and doing so without the confounds of evolved host protective immunity (as expected at emergence), is challenging. … We found a positive linear relationship between pathogen virulence and transmission rate to an uninfected sentinel, supporting the core assumption of the trade‐off hypothesis. Further, in support of the key prediction, there was no evidence for directional selection on a quantitative proxy of pathogen virulence and, instead, isolates of intermediate virulence were fittest. … Our results indicate that selection favors pathogens of intermediate virulence at disease emergence in a novel host species, even when virulence and transmission are not linked to pathogen load.

My point was very simple. What you wrote above I believe to be a strawman, because he seems to have the same assumption that this paper proved:

So the fittest pathogen has a trade-off between virulence and transmission rate. I’ve seen him make no other argument otherwise as I’ve read the book. Please show in his papers where he says otherwise regarding virulence.

The book itself is concentrating on human mutation anyway so far. Have you read it?

This is another topic, but you seem to be equating IFR with virulence. I assume they aren’t the same?

By this definition:

  1. the relative ability of a microorganism to cause disease; degree of pathogenicity.
  2. the capability of a microorganism to cause disease.

Wouldn’t it be correct to say that a disease which causes a two-week illness in one population with a lower IFR and a two-week illness in another population with a higher IFR has the same virulence in both populations? Otherwise, I would like to know how you’re defining this differently or what I’m getting wrong.

But anyway, please cite the reference that shows pathogen fitness changes to something other than this trade-off hypothesis. That is what I was hinting at in the post.

The book is about mutations in general, not just humans. I’ve read the book.

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I agree; I should clarify - it references mutations in general but it’s focusing on human fitness and natural selection so doesn’t get into pathogen fitness so far that I can tell.