Hypothesis: “Flatten the curve” took off because it allows people to participate without 1. signaling they care what happens to them. 2. think things will get bad or 3. think bad things are preventable.
Douglas_Knight
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Georgism
I’m going to write some things about Georgism, prompted by the review of George in the SSC contest. I had a pretty positive view of Georgism before, but had a pretty negative reaction to the review. I have not read George, but it gave me an impression of monomania. It is implausible that land is the root of all evil: of the Irish famine, the 19th century Depression, and modern urban dysfunction. I had first heard of Georgism and LVT for the coordination of modern cities, but I never gave much thought to what it was originally about.
I expect to write a bunch of comments as replies to this comment, which will serve to keep them together. I want multiple comments mainly because I expect to write them on different days and don’t want one to prevent the publication of the other. For good or for ill, this will avoid bridging topics.
That’s a group selection argument.
Although it is widely held by biologists that there is a tradeoff between infectiousness and virulence, people (eg, Paul Ewald) who actually study the evolution of virulence say the opposite, both in theory and data. In the case of sars2, it is overdetermined: death is due to immune overreaction, after the window of selection is over.
Recently I’ve run across several people offhandedly offering disclaimers that they’ve never personally checked that the earth is round. I’ve never thought to check either, but a moment’s reflection reveals that I’ve traveled far enough, both north-south and east-west that the curvature is obvious.
Time zones are a measure of the curvature of the earth. When I travel from New York to California, I know that noon has changed, trusting only my wristwatch. In fact, it was pretty clear to my circadian rhythm. Or just make a phone call to someone you trust on the other coast. Most of the time I don’t discuss sunlight on such calls, but it has come up.
I’ve traveled shorter distances north-south. I’ve been to Glasgow, which is 15 degrees north of NYC. If I went in the spring, there’s probably little to notice, but I went near the solstice, when it was obvious that the nights were much shorter. Similarly, if you go south 15 degrees to Miami, I’m told that the winter and summer day lengths are obviously moderated.
Accurate clocks and instant communication give us a big advantage over the ancients, but the north-south method is largely unchanged.
Added: East-West travel produces a linear effect. North-South travel produces non-linear effects, which can be easy to notice. If I were measuring the height of the sun at noon, that would be linear in the latitude. 15 degrees might be enough to measure without instruments, if I chose to think about it. But the length of the night is not linear. Summer solstice night heads to zero not at the north pole, but just at the arctic circle. So summer solstice in Glasgow was obviously shorter than any night I had previously experienced, maybe cut in half. Whereas summer solstice in Miami is shorter than summer solstice in New York, but just an ordinary length day from other times of the year. Maybe if I had thought to ask the question I could have told the difference without a clock, but I didn’t think about it, whereas the night in Scotland was striking and a topic of conversation. If someone from Miami comes to New York for the solstice, he will experience the shortest night of his life, which might be obvious, but it won’t as dramatic as half the length he’s used to. I knew a guy who moved from Miami to New York and he noticed it, but I think it was about the experience of life, not a single night. There is another non-linear effect as you head to the tropics, which is the solstice shadows at noon shorten to zero. That might be obvious to some people, but it’s not the kind of thing I pay attention to.
All the modeling efforts talked about in the write-up are doomed because they don’t understand the role of the control system
Is that a forward-looking prediction? What consequences was UIUC doomed to? The article ends its coverage of UIUC in early September, declaring it a failure. But, in fact, it achieved its goal of keeping infections below 5k. You could credit that to “the control system,” the panic caused by the early spike that got all the news coverage, but it’s still a success.
If it’s so cheap and easy to make vaccines, why aren’t commercial ones made this way? In particular, the Novavax vaccine sounds similar, so why wasn’t that the first vaccine to market?
Added: Specifically, the ultimate purpose of a vaccine is to get protein into the body. Traditional vaccines grow the virus using its own reproductive apparatus. Fancy new vaccines, like the adenovirus and mRNA vaccines inject instructions and induce the subject to manufacture proteins. But if it’s so easy to just print proteins, why don’t we do that? That’s what Novavax does, unlike the ~7 vaccines that beat it to market.
Added: one difference is that all the vaccines that made it to market, including, I think, Novavax, used the whole spike protein, whereas this proposal uses short peptides. Identifying the right short snippets takes time, while using the whole protein is simpler and more likely to work. The cost of peptides is probably super-linear in length. Still, I remain confused about Novavax.
By default, we should expect viruses to become less deadly over time rather than more severe, but more severe is always a risk. We also believe the new strain carries generally higher viral loads, which could plausibly be a cause of higher severity.
That is the consensus among biologists, or maybe even evolutionary biologists, but the consensus among people who study the evolution of parasites is exactly the opposite. Theory predicts and observation agrees that parasites evolve to become more virulent over time, especially ones that have just jumped from one host to another. See Paul Ewald, for example.
I suspect that Gates had a long-standing specific plan for manufacturing old-fashioned vaccines, but was unable to pivot to funding new vaccines. It’s a lot harder to spend money to speed up deployment of new technologies, especially at arm’s length.
AZ claims this week that the EU negotiations being delayed for a couple months delayed their factories. Why couldn’t they just start earlier? This is a clear claim that money would have mattered. But maybe there is a lot more to this than physical construction. The EU is currently threatening to confiscate AZ vaccine, so maybe AZ didn’t see any point in building factories in countries that hadn’t pre-paid.
Why is the Gates foundation a charity, as opposed to just a non-profit? If he wants to take Buffett’s money and give him a tax benefit, then it has to be charity, but for spending his own money, he doesn’t need this status.
Given the high dimension of the search space, I think (b) is negligible and the linear model (a) of your first comment is better. In low dimension the boundary of the unit sphere is small and you can have a lot of copies on the inside, having to pass through the sphere to reach new terrain. Whereas, in high dimensions, the population will quickly thin out and all be unique, so what matters is the total volume of space explored, not how long it takes to get anywhere.
Dynamically, that predicts that the advantage would rise over time, as a substantial proportion of the population got infected by the original strain. I think we’ve been monitoring the UK variant enough to see that this is not a large portion of its advantage.
Even statically, I think it’s difficult to make the numbers work out. The idea that the population has heterogeneous risk makes a lot of sense, but it doesn’t seem born out by the basic prediction that HIT is much lower than predicted by initial R. I suppose the control system might make it hard to observe how close we are getting to HIT, but I’m skeptical. And you need zero cross-immunity. But then wouldn’t the observed reinfections skyrocket and be obvious? Maybe if the reinfections are asymptomatic, but just as contagious. I guess that this very specific scenario predicts that the new variant has passed through the riskiest portion of the London population and no longer has an advantage there.
My (highly speculative!) hypothesis is that the emergence of these variant viruses arises in cases of chronic infection during which the immune system places great pressure on the virus to escape immunity and the virus does so by getting really good at getting into cells. 11⁄19
That’s plausible, but doesn’t explain why the chronic infections hadn’t done this earlier, and the English strain doesn’t escape immunity in this way (and we don’t know about the others) so I notice it doesn’t feel like it explains things.
That isn’t plausible to me. Not only does it not explain everything, I don’t think it explains anything. There are two traits, immune escape and infectiousness, which is pretty much the same as fitness. It makes sense that chronic infection causes immune escape, but we aren’t looking at immune escape. There might be tons of strains with immune escape out there, but we won’t notice until we achieve substantial herd immunity, at which point they will have increased fitness. If that happens, and we need to explain immune escape in future strains, then this is a possibility. But I see no reason to believe it about these strains. We are filtering by increased fitness, so we need to explain increased fitness. Immune escape is probably a side effect of increased fitness, because it’s a potential side effect of any change.
Fitness is fitness. There is no need for a weird environment to explain selection for fitness, because it’s the main story. In fact, this is exactly backwards. If there is any trade-off between reproduction between hosts and reproduction in hosts, then selection by chronic infection will favor the latter at the expense of the former and probably move away from optimal fitness. Whereas it appears, as Bedford claims, that these mutations are a free lunch. This is quite plausible for a young parasite that hasn’t finished adapting to its new host. But then what does a weird selection pressure explain? Every infection should be an opportunity to develop this. What matters is the number of roughly the number of virus-host-days. A virus trapped in one individual for 100 days is under roughly the same selection pressure as a virus passing through 20 individuals under the same time. I’ve seen a lot of people call that “fast evolution” because 20x as much selection happens in the host, but it’s not any faster in time.
Bedford seems to allude to this view, but he also uses similar points to make a different argument, which is that the UK variant appeared out of nowhere with a lot of mutations, without the intermediate forms being observed. Arising from a chronic infection would explain this. But we also know that all the mutations have arisen before, without seeming to do much on their own. So we know that it only took off when it reached the magic combination, which explains why we didn’t see the intermediate forms. I don’t think chronic infection adds much to this, although I could imagine a scenario in which the individual changes happen to be selected for in chronic infection at the slight expense of general fitness. So it needs the different landscape of a chronic infection to cross the valley and reach the final form. But this seems like excess detail to me.
I don’t believe that every infected cell is killed.
This is about the change that is shared between UK and SA, not about the change in the SA variant that is uniquely worrisome.
That doesn’t distinguish the new vaccines from traditional attenuated vaccines, which also inject nucleic acid into the cell, although inactivated vaccines don’t. Or, for that matter, getting infected. Every year I get a couple of colds, where way more cells get way more nucleic acid than in vaccine.
10% chance of survival is “unlikely” but it’s lives, not warm fuzzies. It may not have been cost-effective, but it was buying something real. (And it may well have been cost-effective if it was marginal use of facilities that already existed.)
10% is the number I have heard for the specific category I have heard triaged against in LA, namely patients whose heart the EMT can’t restart. Instead they can perform CPR to manually pump the heart on the trip to the hospital.
this is 3,809 deaths per day and the average had not at the time been over 2,700 for any 7-day period so far, that that projection was made on December 31, so that seems like a rather bold prediction
If cases are in unprecedented territory, you should expect deaths to go into unprecedented territory. Forecasting deaths 3 weeks in the future should be easy, since it’s forecasting the progression of the disease among people already infected. You just take the number
infectedof cases and multiply by the CFR. At 220k cases/day and a CFR of 1.75%, that’s 3850 deaths/day, so that sounds totally reasonable.(This is all from eyeballing 7-day rolling averages. I got the CFR from comparing the plateau of cases in September to the plateau of deaths in October. I haven’t checked if it has held up or what the lag should be. The 220k cases/day is the 7-day average peak at Christmas. So this requires assuming that the dip after Christmas was an illusion, which has been vindicated by the week since the prediction was made.)
Added: over at Zvi’s blog, Alexander Gordon-Brown claims that CDC does not predict 80k deaths, but that its point estimate is only 64k. Also, that the prediction is dated 12⁄21.
If you make any of these hypotheses precise enough to calculate, then I don’t think that they are likely enough to be worth calculating. The point was just to give suggest how big the space of unknown unknowns is. I think you need an outside view to estimate it. You might hope to get that from the virologists, but they are dismissing it as a “founder effect” which is even more specific, rather than accepting the ignorance of an outside view.
I think I got them all from Francois Balloux, though I’m not sure what he was saying and I may have interpolated a lot of detail. I got 2a and maybe 1 from here. 2b is from here, a response to the first thread. Added: actually, I think I got 2a from the “Does it matter” video, which was generally hostile to
reason and knowledgeepidemiology, but did suggest something like this at the end.
I often hear people claim that Hong Kong and Singapore are Georgist. More specifically, I hear that they have Land Value Taxes. Their success is often attributed to their Georgism.
Hong Kong has a property tax that is not at all an LVT. Singapore has a tax that it claims is a LVT, but it’s really just a property tax that is reassessed when a new building is proposed, rather than complete. I guess that improves incentives, but it seems pretty minor.
There is more to the spirit and letter of Georgism. The central conceit is state ownership of land, which both cities try to monopolize, offering only 99 year leases. I guess this cuts down on long-term “speculation,” but George’s proposals usually seem focused on a shorter term.
The modern account is to emphasize that the value of cities is the positive externalities from all the development. A government should encourage the production of positive externalities, in particular more building. The cities do take this to heart and make it easy to build. Maybe Georgism is really simple and that’s the key point. So many other cities fail it, but it’s not because of failing to grasp the abstract argument for an LVT or the difficult details of implementing it, but because of much more basic and fundamental failure.