1. I have been wondering about the current evidence on mortality rates.
Assuming, as I do, that the death figures are reasonably accurate — I
calculated an upper bound for the number of people dying
of something else while having Covid and being mislabeled in an earlier post — the
uncertainty is the number infected. I gather that the high
estimates of number infected, hence low estimates of the mortality rate,
use the percentage of a random sample who show the relevant antibodies
as evidence of how many have been infected.
But I have seen recent
stories claiming that a large fraction of those who have been infected
don't show the antibodies later. That is being discussed in the context
of the question of whether having had it gives immunity, also relevant
to whether a vaccine is possible. But it's also relevant to the
death rate. If two-thirds of the recovered people fail to show
antibodies, then a death rate calculated from the antibody data is three
times as high as the real death rate.
Are there any competent webbed
discussions of this issue? Anyone here done calculations?
2. I recently had an unpleasant thought about the politics of the response to Covid.
I think everyone agrees that the better the economic situation as of election day, the better the Republicans will do. It follows that Trump would weight economic costs of lockdowns and the like much more heavily, relative to health costs, especially health costs over the next couple of months, than his opponents.
I think everyone agrees that the better the economic situation as of election day, the better the Republicans will do. It follows that Trump would weight economic costs of lockdowns and the like much more heavily, relative to health costs, especially health costs over the next couple of months, than his opponents.
According to which side you are
on, you can describe that either as Trump killing people in order to
make sure he wins the election or the Democrats trashing the economy in
order to make sure he loses.
Of course, health costs also matter for voting, but my guess is that
most people make their decision in terms of the current situation, not
what it was several months earlier. It's even possible that voters judge
by the amount of recent improvement as well as by conditions on
election day, in which case bad conditions, economic or medical, a few
months back, might actually benefit the incumbent: See how much better
things have gotten.
6 comments:
"According to which side you are on, you can describe that either as Trump killing people in order to make sure he wins the election or the Democrats trashing the economy in order to make sure he loses."
Or both.
Immune response to coronaviruses seems to be dominated by T-cells rather than by antibodies, so it may be possible to recover from infection and develop lasting immunity without ever showing positive on an antibody test. The best discussion I've seen online is at Derek Lowe's blog, with particular discussion here, here, and here.
Also, I don't think there's ever been a confirmed case of someone developing symptomatic Covid-19, recovering, and then developing a second symptomatic case. With so many cases of such a high-profile disease, that's a dog pretty conspicuously not barking. Antibody levels may fluctuate in and out of detectability, but it looks like anyone who actually gets sick, gets real immunity lasting for many months at least. If asymptomatic infections also incur lasting immunity, we may be closer to herd immunity than naive antibody testing would indicate.
Many individuals have a T-cell response without a B-cell response, hence no antibodies, but they are cured.
Up to 80 percent of people have natural defense against covid
Where did you see the story that 2/3 of survivors don't have antibodies? I was not able to find such a claim.
Antibody testing in Bergamo found 60% positive. So most survivors have antibodies, at least if you test them soon enough.
https://wattsupwiththat.com/2020/07/27/why-herd-immunity-to-covid-19-is-reached-much-earlier-than-thought-update/
By Nic Lewis
I showed in my May 10th article Why herd immunity to COVID-19 is reached much earlier than thought that inhomogeneity within a population in the susceptibility and in the social-connectivity related infectivity of individuals would reduce, in my view probably very substantially, the herd immunity threshold (HIT), beyond which an epidemic goes into retreat. I opined, based on my modelling, that the HIT probably lay somewhere between 7% and 24%, and that evidence from Stockholm County suggested it was around 17% there, and had been reached. Mounting evidence supports my reasoning.[1]
A key reason for variability in susceptibility to COVID-19 given exposure to the SARS-CoV-2 virus causing is that the immune systems of a substantial proportion (35% to 80%) of unexposed individuals have T-cells, circulating antibodies or other components that are cross-reactive to SARS-CoV-2 and can be expected to provide substantial resistance to it.[6] [7] [8] [9] Such components likely arise from past exposure to common cold or other coronaviruses, or to influenza.[10] Not being specific to SARS-CoV-2, and typically not being antibodies, such immune system components are not normally detected in seroprevalence or other tests for immunity to SARS-CoV-2.
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