Ben writes:
Hi Vincent and Nels,
First, a TWiEvo paper suggestion. A recent study by Dey et al., from Buzz Baum’s lab regarding closed mitosis, its association with nuclear envelope disassembly and the evolutionary implications of this, a fascinating and very TWiEvo suitable read https://www.nature.com/articles/s41586-020-2648-3!
Second, just to throw my two cents in on evolutionary changes in a pathogen’s mortality rate, I think there’s two extra things that are really important to consider. Whether or not a pathogen may evolve to be less lethal is related to whether death is required for, or impacts transmission. To the best of my knowledge, rabies is still uniformly fatal in most mammals despite at least tens of thousands of years of evolution (probably much more), and there seems no trend to lower mortality for rabies. Similarly, many parasites require their host to be eaten for their transmission and so the argument could be made that this could impart a selective pressure towards greater lethality. It is also important to consider if death of the host necessarily means death of the pathogen, many pathogenic bacteria and parasites can also be free living, and so death of the host may not lead to death of the pathogen or alternatively such a small proportion of the total number of organisms of that pathogen infect humans and die out that it has a negligible selective pressure. An example here could be Naegleria fowleri, a primarily free-living organism that rarely infects humans but is extremely lethal.
I loved the discussion from the previous episode, and while I agree that evolving to lower lethality is probably a reasonable general assumption for most single-host obligate pathogens, the influence of mortality on reproduction and transmission should be considered. Trying to predict the future for emerging pathogens is something I love to think about and discuss with friends, and I can’t wait to hear more discussion in future TWiEvo episodes!
Regards,
Ben
Ben Liffner
PhD Candidate – Malaria Biology Lab (Wilson Lab)
Research Centre for Infectious Diseases
School of Biological Sciences
The University of Adelaide
Shinichiro writes:
Hi Nels and Vincent,
I would love to hear a discussion on virulence and transmission in the context of evolution.
It would be very helpful to clarify that virulence (how sick the host becomes) and transmissibility (how well the pathogen spreads) are NOT always selected together.
Virulence and transmissibility are often very difficult to separate even in an well controlled experimental settings:
Does a large plaque indicate high virulence or high transmission on a plate?
What does super enlarged spleen in a mouse indicate?
Host death in 2 days or 10 days when both are 100% lethal, is this due to virulence or transmissibility?
Virulence and transmissibility are confounding factors for sars-cov2-human relationship. The virus is highly transmissible during pre-symptomatic period. The disease is more ‘virulent’ when viral counts wane. This likely means there is no direct selection for virulence.
However, virulence, transmissibility and host-behavior are connected.
Paul Ewald has very interesting discussions.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7118948/
I am hoping he is right and that how we respond public-health-wise may actually reshape the evolutionary trajectory of the covid19 pandemic. Do nothing and maximizing the spread, or mask, distance and be kind to minimize the spread.
I was thinking about this since the spring, and this article came out in Guardian recently.
Stay safe and keep up the fantastic work.
Shin Enomoto, just a biologist who wore multiple hats.