Virulence and vectors

Apropos of nothing, I am reminded of Paul Ewald’s book Evolution of infectious disease (1994). Ewald begins with the question of whether parasites and pathogens evolve towards commensuality (the state of being mutually beneficial, which is what, among others, Macfarlane Burnet thought, along with many immunologists and epidemiologists. Ewald points out that this need not be the case. Consider the following scenario:

The pathogen (P) moves easily between its host environments (E). Assume there are strains that move more slowly to infect new Es (P1, P2) than the “wild type” (P0). If the rate of transmission P2 <P1<P0, then which ones will tend to find more hosts and thus increase in numbers over the others? That is right: P0>P1>P2. Ultimately P0 will tend to sweep to fixation (that is, become the sole strain).

Now assume that the strains vary in how they exploit their Es. If P0 is less aggressive at tying up the replication machinery it needs to survive and reproduce – whether it is a virus using the cell replication machinery, or a bacterium eating cells and other resources, or a parasite that eats the host’s tissues; it doesn’t matter), then if the rates of transmission are equal, the more aggressive strains (P1 and P2) will out breed it.

The end result is that which ones succeed in supplanting the others, or whether there is an evolutionarily stable strategy where they reach and hold an equilibrium mixture, depends on the values of the rate of transmission (the vector*) and the aggression of exploitation (the virulence).

Suppose P0 is most virulent and has the highest vector. It wins outright. Suppose P0 has the highest vector and P2 the highest virulence, though. In this case it depends very much on how the two cancel each other out. In evolutionary terms, it depends on the relative fitnesses.

Now organisms (the host environments, from the point of view of the pathogen) have their own reactions to this. One is to activate the immune system to destroy the infection and thus reduce the success of virulence. The other is to change the frequency of transmission by behaviour, or by genetic mutations if they occur. Either reduces the fitness of highly virulent/high vector pathogens. In general, the closer a pathogen’s transmission rate from one host to another is to the host’s own reproductive frequency, the closer the fitness of the dominant strain approximates that of the host. In less roundabout words, if you make it harder for a pathogen to spread, you favour the strains that are less virulent. Why? Because the ones that kill or overexploit their hosts do not tend to be spread as quickly once the host population decreases, because their hosts are dead and thus not infectious after a while.

So commensuality will evolve only when the genetic interests, or fitness, or the host and pathogen tend to coincide.

This need not always happen. Depending on the values for virulence and vector a pathogen can continue to be pretty nasty, and of course new strains exploit hosts in new ways. But this does suggest another reason for “flattening the curve”: in addition to making the health system itself able to deal with the increase and peak of cases, it makes those strains that are highly virulent less fit, and so it encourages the evolution of the pathogen P towards low virulence. Failing to take steps to slow the rate of infection will lead to a higher virulence in the longer term.

I hope this helps some of you think about this in evolutionary terms. We are not only the host environments for pathogens, we are reactive systems. Practising hygiene is something other ecosystems cannot do to over-exploiting parasites like us.

• Yes, I know that a vector in epidemiology is the means by which a pathogen is transmitted, how else will I get the alliteration?

Ewald, Paul W. Evolution of Infectious Disease. Oxford [England]; New York: Oxford University Press, 1994.

Image from https://medicalxpress.com/news/2017-06-global-flu-evolution-person-infection.html

Errors introduced by autocorrect corrected manually