The New York numbers are certainly interesting. I wonder if New York reached a no-longer-susceptible rate that means that it can no longer support long transmission chains in lockdown...
Claim is that European strain, which is also in New York (and I’m going to presume New Jersey and other surrounding areas as well, because physics), is deadlier than the strain elsewhere, generating orders of magnitude more viral load.
I am VERY VERY skeptical of this paper.
The mutations they show are TINY. And their methods section does not include any details at ALL of how they grew their viruses, or how they diluted them to a multiplicity of infection of 0.5. Short version, they were supposed to grow cultures of each of their 11 viral isolates, measure how infective each culture was, and then dilute them so there were 50% as many infective viruses as cells in the flasks they poured them into to make sure they all started from the same point. But they give no details of how they measured this and did the dilution.
When growing viruses, batch effects are a BITCH. Your virus culture might be a little differently diluted, they might be a different average age, or your culture might’ve been produced in a corner of the incubator that was a little warmer. The lines of each of the viruses bounce around over time, some higher and lower over time, and all I really see is a cloud of viral RNA levels that goes forward over time with some high and some low at any given time. They have four replicates of each virus and DO show that the replicates behave exactly like each other, but their methods section doesn’t say if they took the same diluted virus stock and put it into four culture flasks, or made four separate stocks of each virus. It is QUITE QUITE possible that they are just seeing differences in the stocks they grew that have to do with their culture histories and dilution details, rather than genetic differences.
On another point, the cell line they grow them in isn’t even human and doesn’t really have an innate immune response, which would be by far the most important things regarding real-world infection. Their high viral replication lines were also not from their more severe cases.
They definitely did find ONE interesting thing—one of their isolates appears to have independently invented a particular missense mutation seen in another strain elsewhere in the pile of global sequences. Actually suggestive of selection. It’s not in the receptor binding domain of the S protein though, so it shouldn’t affect binding or immunity much.
Other papers have found MUCH more interesting mutations—there is a cluster of cases in Singapore that have up and completely lost one of the accessory proteins of the virus, which is involved in squashing the human innate immune response, and another case in Arizona has broken another such accessory protein beyond repair. This is presumably because this bugger evolved in bats, and their interferon response is on a freaking hair trigger. The anti-immune-system measures of the virus are overclocked relative to what you need to replicate in humans, and losing some of them doesn’t really hurt them.
The New York numbers are certainly interesting. I wonder if New York reached a no-longer-susceptible rate that means that it can no longer support long transmission chains in lockdown...
I am VERY VERY skeptical of this paper.
The mutations they show are TINY. And their methods section does not include any details at ALL of how they grew their viruses, or how they diluted them to a multiplicity of infection of 0.5. Short version, they were supposed to grow cultures of each of their 11 viral isolates, measure how infective each culture was, and then dilute them so there were 50% as many infective viruses as cells in the flasks they poured them into to make sure they all started from the same point. But they give no details of how they measured this and did the dilution.
When growing viruses, batch effects are a BITCH. Your virus culture might be a little differently diluted, they might be a different average age, or your culture might’ve been produced in a corner of the incubator that was a little warmer. The lines of each of the viruses bounce around over time, some higher and lower over time, and all I really see is a cloud of viral RNA levels that goes forward over time with some high and some low at any given time. They have four replicates of each virus and DO show that the replicates behave exactly like each other, but their methods section doesn’t say if they took the same diluted virus stock and put it into four culture flasks, or made four separate stocks of each virus. It is QUITE QUITE possible that they are just seeing differences in the stocks they grew that have to do with their culture histories and dilution details, rather than genetic differences.
On another point, the cell line they grow them in isn’t even human and doesn’t really have an innate immune response, which would be by far the most important things regarding real-world infection. Their high viral replication lines were also not from their more severe cases.
They definitely did find ONE interesting thing—one of their isolates appears to have independently invented a particular missense mutation seen in another strain elsewhere in the pile of global sequences. Actually suggestive of selection. It’s not in the receptor binding domain of the S protein though, so it shouldn’t affect binding or immunity much.
Other papers have found MUCH more interesting mutations—there is a cluster of cases in Singapore that have up and completely lost one of the accessory proteins of the virus, which is involved in squashing the human innate immune response, and another case in Arizona has broken another such accessory protein beyond repair. This is presumably because this bugger evolved in bats, and their interferon response is on a freaking hair trigger. The anti-immune-system measures of the virus are overclocked relative to what you need to replicate in humans, and losing some of them doesn’t really hurt them.