CWD research

[Hunting Wife]

If mature bucks have higher % of desirable resistant genes wouldn’t managers want to manage for higher % of mature bucks? The older bucks that survive CWD, harsh winters, drought, predators, and carry the very best genes likely are the healthiest critters on the mountain that have exactly what it takes to endure harsh conditions.

Not necessarily, because what they are saying in this paper is that the higher frequency of resistant genes in older deer appears to be an artifact of attrition (all the wild type ones died earlier) vs showing any type of actual genetic shift due to selection in the population. Those bucks are not passing that genotype on to the new fawn crops at any higher frequency now than they did before, which is the interesting part that seems to be counter to what you’d expect under natural selection. In every new fawn crop, the distribution of genotypes is almost exactly the same as it was when they sampled before. I’ll have to read it again when I have more time to digest, but that was what stuck out to me.

Given that the age structure of the population has not significantly changed, and that it appears slightly skewed towards younger animals already (at least for a population that is not hunted) I wonder if the extra life span (generally just months) conferred by the resistant genotype just isn’t enough to convey a selective advantage? Or if it is, it might take a much, much longer time scale for a disease that operates on such a (relatively) long time scale?

They are also not accounting for immigration. That could potentially be a large influence and it didn’t sound like that was included in their model. Its possible that could be helping stabilize things (both genetics and population numbers) somewhat, but it would be nice to have some kind of data. I’m not familiar with the area so can’t guess.

I don’t know. Brings to mind more questions than answers. But again, really interesting paper.

 

[Laszlo Cravensworth]

Not necessarily, because what they are saying in this paper is that the higher frequency of resistant genes in older deer appears to be an artifact of attrition (all the wild type ones died earlier) vs showing any type of actual genetic shift due to selection in the population. Those bucks are not passing that genotype on to the new fawn crops at any higher frequency now than they did before, which is the interesting part that seems to be counter to what you’d expect under natural selection. In every new fawn crop, the distribution of genotypes is almost exactly the same as it was when they sampled before. I’ll have to read it again when I have more time to digest, but that was what stuck out to me.

Given that the age structure of the population has not significantly changed, and that it appears slightly skewed towards younger animals already (at least for a population that is not hunted) I wonder if the extra life span (generally just months) conferred by the resistant genotype just isn’t enough to convey a selective advantage? Or if it is, it might take a much, much longer time scale for a disease that operates on such a (relatively) long time scale?

They are also not accounting for immigration. That could potentially be a large influence and it didn’t sound like that was included in their model. Its possible that could be helping stabilize things (both genetics and population numbers) somewhat, but it would be nice to have some kind of data. I’m not familiar with the area so can’t guess.

I don’t know. Brings to mind more questions than answers. But again, really interesting paper.

Potential that the extended lifespan of the resistant genome occurs significantly after the breeding season.

WAG: but it could be that a large portion of CWD mortality is post rut, so those infected resistant bucks would still be competing with non resistant bucks for breeding opportunity. Non resistant bucks die of winter kill in January and resistant bucks die in March, no selective benefit is conferred to the offspring.