4 ms·

"...probably due to a genetic mutation in the virus which has not yet been demonstrated scientifically." -- you can stop reading once you get here. It's not tha

"...probably due to a genetic mutation in the virus which has not yet been demonstrated scientifically." -- you can stop reading once you get here. It's not that hard to find out if there was a mutation in the virus, you sequence it and compare it. If you didn't find any differences it means we probably got better at handling COVID19 - IE: earlier hospitalization, better care - rather than a weaker virus.

Amorymeltzer 6y ago
I agree that you can stop reading, but not with your rationale. >It's not that hard to find out if there was a mutation in the virus, you sequence it and compare it. There are lots of problems with this assumption. Sequencing is pretty quick, it's not instantaneous or free. More to the point, sequencing a single virus from a single individual who survived doesn't necessarily tell you anything about that virus. You would need to sequence many viruses from many patients, and compare patient outcomes (while controlling for other factors) with sequence data. That is neither quick nor easy. Viruses can mutate quickly. From what I've read, SARS CoV2 doesn't appear to have a high mutation rate compared to other viruses more in the zeitgeist, but it's definitely much higher than, say, the typical mammal. That not only means that sequencing is harder, but it also means there will be multiple strains to compare. There isn't one virus: there are currently thousands (https://nextstrain.org/ncov/global https://nextstrain.org/ncov/global) of genomes publicly available, so there's a lot to look at. Finally, the point the individual being quoted was making is that, after all that work, the best you're likely to come up with is "there are a handful of sequence changes that correlate to better outcomes." You haven't proved it ("demonstrated scientifically"). The reason you can stop reading here is that this is one person speculating, seemingly based off of anecdotal data. They have some authority and it's implied they are looking at a lot of data, but there are no hard stats or facts.

Amorymeltzer 6y ago

I agree that you can stop reading, but not with your rationale. >It's not that hard to find out if there was a mutation in the virus, you sequence it and compare it. There are lots of problems with this assumption. Sequencing is pretty quick, it's not instantaneous or free. More to the point, sequencing a single virus from a single individual who survived doesn't necessarily tell you anything about that virus. You would need to sequence many viruses from many patients, and compare patient outcomes (while controlling for other factors) with sequence data. That is neither quick nor easy. Viruses can mutate quickly. From what I've read, SARS CoV2 doesn't appear to have a high mutation rate compared to other viruses more in the zeitgeist, but it's definitely much higher than, say, the typical mammal. That not only means that sequencing is harder, but it also means there will be multiple strains to compare. There isn't one virus: there are currently thousands (https://nextstrain.org/ncov/global https://nextstrain.org/ncov/global) of genomes publicly available, so there's a lot to look at. Finally, the point the individual being quoted was making is that, after all that work, the best you're likely to come up with is "there are a handful of sequence changes that correlate to better outcomes." You haven't proved it ("demonstrated scientifically"). The reason you can stop reading here is that this is one person speculating, seemingly based off of anecdotal data. They have some authority and it's implied they are looking at a lot of data, but there are no hard stats or facts.