Nature Journal Club

Carl Bergstrom

University of Washington, Seattle, Washington

An evolutionary biologist considers the virulence of emerging infectious diseases.

When a pathogen — for example, HIV — emerges into the human population, it adapts to growth and transmission in human hosts. At the same time, its virulence (often measured by case mortality) typically changes as well. On the basis of theoretical arguments and examples such as the myxoma virus, conventional wisdom holds that if a disease is highly virulent at first, it will rapidly evolve reduced virulence so as to maximize transmissibility. The idea is that pathogens face a virulence–transmissibility trade-off: strains that kill or even incapacitate their hosts are unlikely to spread as broadly as those that keep their hosts alive and mobile.

One might think — and some have argued — that we can take comfort from such reasoning. By this logic, the 60% mortality rate seen in human cases of H5N1 avian influenza should rapidly attenuate were a human pandemic to occur. But in the inaugural issue of Evolutionary Applications, Bull and Ebert refute this thinking using a clear, simple mathematical model (J. J. Bull & D. Ebert Evol. Appl. 1, 172–182; 2008).

As someone working on the dynamics of emerging infectious diseases, I find this paper fascinating and sobering in equal measure. The gist of its argument is that trade-off models may not apply well to emerging infectious diseases, precisely because they are still emerging. When a disease first enters a new host, it can be far from the optimum point on the virulence–transmissibility trade-off curve. Its early evolutionary trajectory may be contingent on mutation supply and thus very hard to predict: virulence might decline, but could also initially rise.

The implications are clear. We need to invest now in disease surveillance, public-health infrastructure and pandemic planning. We cannot count on evolution to do our work for us.

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