It seems that both historically and currently the first order response is quarantine and travel restrictions to prevent potential transmission. Pretty sensible as we have plenty of reasons and plenty of evidence supporting the travel and trade spreads diseases to new locations.
But is that really the same when we’re talking about mutations of an existing virus that is widespread? I’m not entirely sure, hence the post. Hence the rather speculative post I should probably say.
I would imaging the starting point to such a question just might be “So just what is the mutation process?” That seems to be somewhat poorly understood—but I’m hardly well informed here.
Mutations come in many forms but we might put them into one of three buckets: “advantage” gained, no effect (neutral mutation?) and “this just broke everything”. The first is really what most are concerned with here and what the Delta and Omicron mutations are really about.
In general it seems these are largely taken as just random events. I think that view is what underlies the idea that one can (in theory I suppose) trace these variants back to an original host from which the new dominant strain emerged.
The remarkable capacity of some viruses to adapt to new hosts and environments is highly dependent on their ability to generate de novo diversity in a short period of time. Rates of spontaneous mutation vary amply among viruses. RNA viruses mutate faster than DNA viruses, single-stranded viruses mutate faster than double-strand virus, and genome size appears to correlate negatively with mutation rate. Viral mutation rates are modulated at different levels, including polymerase fidelity, sequence context, template secondary structure, cellular microenvironment, replication mechanisms, proofreading, and access to post-replicative repair. Additionally, massive numbers of mutations can be introduced by some virus-encoded diversity-generating elements, as well as by host-encoded cytidine/adenine deaminases. Our current knowledge of viral mutation rates indicates that viral genetic diversity is determined by multiple virus- and host-dependent processes, and that viral mutation rates can evolve in response to specific selective pressures.
Emphasis added in the above quote. Huh? Virus may actually have evolved structures that seek to produce mutations?
I have recently read a different article (forget the link but it was not a peer-reviewed publication yet but seemed like reasonable thinking) regarding the value of travel restrictions. Their model indicated that local spread will dominate any imported spread from travelers so such restrictions are not really effective or necessary. Makes sense . . . unless you’re talking about a new version that is not local . . . unless the view that the new version only emerges in one place (p for simultaneous emergence separately near 0) is wrong.
We also tend to see reported new variants of SARS-COV-2 and then it’s found in other location—generally to a lessor degree. That patter certainly is consistent with an one origin view. But we also hear about cases where no good connection exists. Isn’t that also consistent with a virus that has structures designed to test mutations (and probably not entirely randomly) having just emerged around the same time locally? Is there perhaps a reason to think such mutations might well emerge on a similar timeline rather than these just being random where the p(A) and p(B) -- A and B being the locations seeing the mutation—is basically 0?
I want to say this question about a mutation emerging in multiple locations rather than just in one and then spread has been touched on here but not certain (and have not tried searching). Regardless of that point though, can we really have a rational response to mutations without having some answers here? I’m not sure we have them but that could be my ignorance. But if we actually do have reasonably good answers here I would think an organization like WHO, which seems to be calling for lighter/no travel restrictions on SA and other countries reporting Omicron, should be pointing something like that out.
Viral Mutation, Pandemics and Social Response
It seems that both historically and currently the first order response is quarantine and travel restrictions to prevent potential transmission. Pretty sensible as we have plenty of reasons and plenty of evidence supporting the travel and trade spreads diseases to new locations.
But is that really the same when we’re talking about mutations of an existing virus that is widespread? I’m not entirely sure, hence the post. Hence the rather speculative post I should probably say.
I would imaging the starting point to such a question just might be “So just what is the mutation process?” That seems to be somewhat poorly understood—but I’m hardly well informed here.
Mutations come in many forms but we might put them into one of three buckets: “advantage” gained, no effect (neutral mutation?) and “this just broke everything”. The first is really what most are concerned with here and what the Delta and Omicron mutations are really about.
In general it seems these are largely taken as just random events. I think that view is what underlies the idea that one can (in theory I suppose) trace these variants back to an original host from which the new dominant strain emerged.
Emphasis added in the above quote. Huh? Virus may actually have evolved structures that seek to produce mutations?
I have recently read a different article (forget the link but it was not a peer-reviewed publication yet but seemed like reasonable thinking) regarding the value of travel restrictions. Their model indicated that local spread will dominate any imported spread from travelers so such restrictions are not really effective or necessary. Makes sense . . . unless you’re talking about a new version that is not local . . . unless the view that the new version only emerges in one place (p for simultaneous emergence separately near 0) is wrong.
We also tend to see reported new variants of SARS-COV-2 and then it’s found in other location—generally to a lessor degree. That patter certainly is consistent with an one origin view. But we also hear about cases where no good connection exists. Isn’t that also consistent with a virus that has structures designed to test mutations (and probably not entirely randomly) having just emerged around the same time locally? Is there perhaps a reason to think such mutations might well emerge on a similar timeline rather than these just being random where the p(A) and p(B) -- A and B being the locations seeing the mutation—is basically 0?
I want to say this question about a mutation emerging in multiple locations rather than just in one and then spread has been touched on here but not certain (and have not tried searching). Regardless of that point though, can we really have a rational response to mutations without having some answers here? I’m not sure we have them but that could be my ignorance. But if we actually do have reasonably good answers here I would think an organization like WHO, which seems to be calling for lighter/no travel restrictions on SA and other countries reporting Omicron, should be pointing something like that out.