I HAVE TO plug Suzana Herculano-houzel’s book “the human advantage” and all the research she and her group have done since it was published.
Short version: as you scale up a generic vertebrate brain, it only has 4x as many neurons every time it increases in mass by a factor of 10. (A factor of 16 after 100, etc). There are two clades that break this relationship: primates and birds, both of which have a 1:1 relationship between brain size and neuron number. The primate density is about the density of a mouse brain, and bird brains are 6x as dense as this. A large primate brain is much more impressive than a large mammal brain. You get that elephants have brains about as impressive as chimps, and big whales have brains as impressive as late homo erectus—both of which I think make sense. Humans show up as having 4x the neurons of chimps/elephants and ~2x that of the biggest whales.
Human brains also appear to just be scaled-up primate brains, with the size of every brain region falling RIGHT on the trendlines of every other primate. I am skeptical of our subspecies being significantly smarter in any general way than other hominids with similar brain sizes.
Indeed, I would call complex culture ‘a thing that happens in large and dense enough human populations’ rather than ‘something humans do’. There is a case study in Australia—Australia and Tasmania were separated by water at the end of the last glaciation, and ten thousand years later the population in Tasmania was very very low and they had lost most of the tools that the Aboriginal people of Australia had. It’s a percolation problem—with enough people and dense enough people you get reliable transmission of culture down the generations, and new innovations stick. I would argue that this, not intrinsic differences in cognition, is probably why Neanderthal toolkits stayed simple longer, they were living in the cold wastelands of Europe and Asia and genetics indicates they went through a LOT of low-population bottlenecks compared to our straightforward single bottleneck and expansion.
It should be noted that a big part of smallpox variolation was not the viral dose, but the means by which it entered the body—a scratch instead of an orifice.
From what I have seen, ICU patients are less focused in the elderly than deaths are. The chance of winding up in the ICU for a 30 year old appears to be 1.5+ %. I doubt that leaves the lungs unscathed, or with the same vulnerability to future insults.
Very first serology data is coming out. 164 close contacts tested by PCR and serology. 16⁄164 of contacts PCR+ & all PCR+ also serology+. Additional 7⁄164 were serology+ but PCR-. Overall 23⁄164 close contacts + in at least one test; 10⁄23 were asymptomatic. Only about half of people show no symptoms, the rest show the spectrum of reported symptoms as spoken of before. The hope for widespread transmission and flulike death rate is gone.
Very first serology data coming out.
164 close contacts tested by PCR and serology. 16⁄164 of contacts PCR+ & all PCR+ also serology+. Additional 7⁄164 were serology+ but PCR-. Overall 23⁄164 close contacts + in at least one test; 10⁄23 were asymptomatic.
Asymptomatic fraction circa 50%. Upper range of what I thought likely. Not the vast majority at all. Actual death rate in the normal population most likely circa 0.6%.
I would expect a pronounced policy push towards national self-sufficiency wherever possible for drugs, medical equipment, and probably other strategically-important things. I would also suspect major pushback against just-in-time supply chains with little in the way of warehoused inventory.
Very positive developments to my mind! Nothing biological operates on such slim margins and such high efficiencies as much of industrial civilization. Because everything that did died, and those with more in reserve and with more distributed capacity were more robust and survived.
The United States owns its own central bank and printing press. The only way it would ever default is if it chose to do so. The central bank can buy up however many bonds it wants with new money, and the mint can do creative tricks to create as much of its own money as it wants.
The latest professionals are suspecting a total infection-to-death rate of a normal population (not a cruise ship) of ~0.6%.
On the Diamond Princess it was reported that 20% of positives never showed symptoms, and Korea is reporting 30%. So some of those asymptomatics will probably progress, but not all.
These numbers support my suspicion that >10% of North Italy has already been infected, with a death rate of ~1%.
Brook’s response is pretty good. I can provide a little more detail.
The spike protein of the virus both mediates binding to the ACE2 protein (which allows it to attach to the cell in the first place) and the fusion of the membranes. ACE2 is not involved in the fusion event, that is completely mediated by the spike, all ACE2 does is allow binding that brings the two membranes close together for a long time. The spike has two functional domains, one that is highly variable across coronaviruses that mediates attachment and is the reason different viruses attack different species and cell types, and one that is more highly conserved that triggers the membrane fusion. In order for the fusion to occur, the spike protein has to be processed by a protease that actually cuts the fusion domain apart from the binding domain. This does not make them fall off each other, they remain bound, but they no longer have a continuous backbone. This then allows a re-folding of the protein to a lower-energy state, which drives the fusion of the closely opposed membranes.
It appears from the literature I have found that the re-folding requires an acidic pH, suggesting that fusion probably requires endocytosis of the virus into the lysosome as it goes along for the ride with recycled ACE2 protein. (This is one of several reasons that chloroquine and hydroxychloroquine are being studied for efficacy, they are known to reduce the acidification of this cellular compartment.) They are still arguing about if the current virus has the spike protein cleaved during synthesis, or cleaved by proteases that are present in the lysosome where the ACE2 is recycled. One of the distinguishing characteristics of this virus compared to other coronaviruses is extra cuttable sequences between the two domains allowing more proteases to more easily cut the two domains apart, causing faster and more reliable viral entry. This has been noted in virulent strains of multiple other viruses in the past.
That’s gonna take a lot of experiments on monkeys to get the answer to...
I did look at the Iceland data. I divided the NUHI positive tests by the total tests, and saw a very noisy upwards-trending line in the fraction of positive test results.
As for hospitalizations, I was comparing the age distribution of hospitalizations for flu and confirmed covid. I found that the ratio of 20-45:65+ hospitalizations for flu was 1:7, and that the same ratio for covid was 1:2. Assuming a similar age distribution for actual infections, this means a larger fraction of young people is coming down with severe disease.
As for ICU periods, doctors are reporting that many covid patients require a ventilator for 1-2 weeks. https://www.nbcnews.com/health/health-news/what-ventilator-critical-resource-currently-short-supply-n1168641
I am looking for the resource I read yesterday that the typical flu ventilation period was 3-4 days.
Contact tracing and isolation empirically does work, since places that did them did not need to go into the severe lockdowns that stopped spread elsewhere. It would not empirically work if most people were asymptomatic. Additionally, if most cases were asymptomatic or weakly symptomatic there would be few cases of multiple close contacts becoming ill. These are common. There’s even a case study of 45 out of 60 members of a choir all becoming ill at once...
Asymptomatic transmission is definitely happening, both in the period before symptoms appear and in the 20-50% of people who do not show symptoms. Contact tracing catches these people once one of their contacts—that gave it to them OR got it from them—becomes visible and all their contacts are quarantined.
The decline in fevers is probably mostly flu going away, with a lower replication number that requires less distancing to die out.
Yes I am.
News reports, which are usually behind reality, indicate >1000 out of ~1800 ICU beds in the city (which normally run at ~80% capacity for literally everything else) are currently occupied by Covid patients and that it is rising at >30% daily.
Paramedics are scrambling, responding to more calls daily than on 9/11.
How can the ICU admission rate be similar to the flu, when fever levels (healtweather.info) in New York are lower than the peak of flu season but they are strapped for space?
This would not be consistent with them having gotten the spread under control and stopped without lockdowns.
Yes, if they were missing lots of asymptomatic contagious people, they would not have gotten their outbreak under control. If we assume a few asymptomatic locked-down contacts had false negatives, their numbers are approaching the numbers you would expect given the Diamond Princess data. I cannot see a situation in which there could plausibly be a huge number of missed asymptomatic people given these two data sets...