It does seem that close contacts of infected people acquire T-cell immunity even without infection, but at least 90 days after exposure there does not seem to be a decreasing trend: https://www.nature.com/articles/s41467-021-22036-z
Have you or anybody else sensibly written about the P1 variant in Manaus? Despite a prior infection rate of ca. 75% in January, Manaus not only experienced a surge in new infections, but also a record high in hospitalizations. This is evidence against the usual assertion that T-cell immunity will provide enough protection against new variants that we will not have to worry about Covid-19 anymore once 70% are vaccinated.
Agreed. In addition, the quoted article is summarizing the policy incorrectly it seems: They write that the school will be closed when there is no evidence of in-school transmission, but that is wrong: if contact tracers find the source as outside of the school, the school will (presumably) not be closed.
So if the model is true, one potential source of temporal variation might be waning immunity acquired after being exposed but not infected. Will link studies later, but many non-infected people show some T-cell responses against Sars-Cov2. In this scenario, e.g. a doctor gets coughed on, gets lucky, and develops some sort of temporal immunity that protects them for the next few months. After some time though this protection wanes and their risk increases again (this would probably not be a binary but continuous process).
I know too little about immunology, but afaik T-cell immunity wanes very slowly, so it does not quite fit the mark. Maybe there are other forms of immunity/antibodies that would explain this better.
Very interesting model, thanks for writing this up!
I will have to think about it in more depth. How do settings fit into this scenario where we know that basically everyone (50-75%) gets infected in an arguably short time frame: meat plants, close living quarters or prisons?
This is an interesting hypothesis, but I find it implausible that there is large temporal variation in vitamin D levels. Seasonal variation which might be even the biggest factor affects everybody the same, and it just does not seem to match my experience that the majority of the population changes their diet in such random ways that they could become Vitamin d deficient by chance. Same with indoor/outdoor activities, most people's life is not that variable that they are spending each day outside one month, but not the next. Besides, Vitamin D deficiency is correlated very strongly with various commodities, which definitely do not randomly fluctuate.
I would also bet that the secondary household attack rate is similar across different age groups (except children) while it is known that Vitamin D deficiency is much likelier in older people.
This is right. For people who do not know, you cannot actually use AMD GPUs for deep learning (at least not productively, AMD is trying to get there though), so AMD's rise has little to do with AI.
This is the key point. All other comments are about the base rates of general forms of thrombosis, but the concern is about a rare, special type. It is actually not inconceivable that the risk of death for young people from this vaccine might be higher than the risk from Covid-19.
AstraZeneca is not a RNA based vaccine, so does not contain any LNPs as far as I know.
Yes, but only if you do it early enough. By the time you are PCR positive I would assume it is already too late.