I saw this in another thread:
And I wondered. I’m seeing higher replication numbers for the ‘UK strain’. Either that means that people are less resistant ---- or that carriers are more infectious.
Mostly there seems to be an assumption that people are less resistant (perhaps there is a lower level of pre-existing immunity), but I haven’t yet seen any study that answers the question.
We’re talking about one metric - the probability that an infected person passes the disease on to another person. It seems to me that there is no distinction between the infected person being “more infectious” and the target being “less resistant”. They are exactly the same thing.
[posted by mistake before I finished]
But I guess what you’re getting at is the mechanism for why the probability is higher. Could be higher viral load, something about the transfer process, pre-existing immunity, etc.
If a particular strain is more infectious, that could be because more people become infectious, or that people who become infectious release more virus, or that people who come in contact with the virus are more likely to be infected.
These are ‘exactly the same thing’ in the same way that Riemann is ‘exactly the same thing’ as Joe Biden, but it’s still an interesting and important distinction.
I have not noticed “people are less resistant” as a common explanation for why we’re supposed to be nervous. “More infectious”, which captures both your directions, is what’s almost always used.
Eta: and you took my quote in a weird place in your OP. I meant any random individual you happen to meet, including covid positive people who aren’t necessarily infectious.
Posted before the second half of Riemann’s reply showed up. I note that both halves were posted at the same time, but somehow …
IMO … At the moment given current knowledge, as @Riemann says it’s a distinction without a difference.
But if we knew whether the problem was greater spreadability or greater susceptibility that might drive our countermeasures in different directions. IOW, should we be controlling the output or the input side of the infection chain?
So it will be desirable to figure that out pronto.
I agree in principle, but the only aspects that would be a crucial priority would be where we they would have some practical influence on the countermeasures. The obvious one is variation in immune response to the existing vaccines, which is already being analyzed as a very high priority.
What other aspects would affect social policies where the current priority is masking and social distancing? Maybe evidence of surface transfer, which isn’t apparently significant for the initial strains. But I think people are already if anything too focused on sanitizing fomites, when the evidence is that by far the highest priority is to minimize the possibility of aerosol transfer.
Why only be interested in practical influence and crucial priority? Some of the rest of this stuff is interesting science.
Maybe I should have posted in General Questions instead of QZ.
Afaik, all the talk about “more infectious” is from looking at the spread numbers. I don’t think anyone is claiming “this mutation makes people more susceptible” or “this mutation makes prior immunity less effective”. I don’t think there’s a GQ answer, atm.
I haven’t seen an answer, which is why I posted the question. But “nobody has answered this scientific question” is different than “there is no answer to this philosophical question”.
I’m not sure what philosophical question you’re referringto.
It could also mean that new cases happen to be predominantly UK variant, merely by luck ofnthe draw. Even when total active cases are dropping, new cases are still coming. If someone comes back from a party weekend in London and goes right back to their job at the meatpacking plant, that might be the main source of new cases. Especially when everything else is in lockdown.
I didn’t say I wasn’t interested. Why do you perversely find it difficult to understand why somebody would comment on the fact that limited research resources are going to be prioritized in the middle of a pandemic?
Is it unreasonable to respond to postings in this thread as if they are attempts to address the thread subject? If you are deliberately changing the subject, why perversely post in this thread?
“Why Q?”
“Z isn’t happening”
“Yes, but Why Q?”
“Z isn’t a real subject”
“Yes, but Why Q?”
“Why do you perversely object to postings telling you about Z?”
“Because if I wanted to ask about Z, I would have posted a different question.”
I’ve got to strongly agree with @Riemann. What you want to discuss doesn’t make sense. Exactly why the variants may be more contagious is months of research that’s yet to be done. Your gut impression that “Mostly there seems to be an assumption that people are less resistant” is entirely in your own head, as far as I know. If you can’t back that up, what’s to discuss?
Not to challenge you here, but I’m wondering where to find the replication numbers you’re seeing. My impression has been that some initial story/model came out about the strain being more infectious and it’s been circulated as something akin to fact since then, but that there’s not yet been any rigorous scientific studies that come to that conclusion (and perhaps nor could there be, absent experimental trials, given all the confounders).
I didn’t save the citation – just some random news article quoting a government COVID spokesman saying something like ‘we’re seeing replication numbers like 0.98 instead of 0.6’ (Those would be replication numbers after making lockdown/social restrictions, and would justify stricter lockdown)