https://tamino.wordpress.com/2020/06/21/covid-19-red-states-blue-states/?fbclid=IwAR3KVvtr7aS1MUtu9r0A8SGv8csQRIEvLf6SSg_pP9judQSznClRUoRf4yQ

Covid-19 in Sweden:

https://www.covid19insweden.com/en/

Linked to the preprint DOI here:

https://gregladen.com/blog/2020/05/04/how-the-pandemic-ends/#comment-873180

https://getpocket.com/explore/item/coronaviruses-a-brief-history?utm_source=pocket-newtab

In case you missed it the first time:

https://gregladen.com/blog/2020/04/30/problems-conceptualizing-covid/#comment-873089

https://news.yahoo.com/mutant-coronavirus-emerged-even-more-110046843.html?soc_src=hl-viewer&soc_trk=fb

Tyvor, from a couple of sets each of a few hundred genes and recombinations of parts of gene sequences, the body during fœtal development builds T cell and Be cell clones whose receptors are each specific for particular/different antigens. With a lego-like rearrangement of the receptor genes/sequences, and from combinations of resulting protein monomers, in the order of 10 million different clones or more can be generated from the original few hundred genetic templates.

These clones loll about the body (it’s more complicated than that, but you get the picture) with their receptors expressed on the surface of the cells. If they encounter their particular target antigen for the first time (a random process) they are activated to reproduce, and in the case of B cell the receptor is also expressed in slightly modified form as soluble antibodies. These actived cells do their jobs mopping up the intruder, and then develop a primed pool of resting cells that will respond more quickly on subsequent re-challenge.

It’s energetically/volumetrically inefficent to have every possible clone pre-primed, hence the two-stage process. And it’s hellishly more complicated than this. But in a nutshell that’s how it works.

Greg, as you say there’s nothing wrong with titres declining over a couple of years. The issue is whether they decline so much that there’s little effective specific immunity after 12-24 months, or if there’s still sufficient immunity to prevent serious symptoms and to keep the successful shedding of virus sufficiently low that the basic reproductive rate is near or below 1.

In a viral disease model where there’s high contagiousness and appreciable mortality, such differences in the duration of effective immunity can make a significant difference.

My wife is a teacher. I think this idea is dangerous nonsense.

I have an asthmatic daughter who is a teacher also twin daughters who are at the drip face as are the twin daughters (granddaughters) of one of them. I find RickA’s take on this topic irresponsible at best.

RickA should really study ‘Deadliest Enemy: Our War Against Killer Germs’ by Michael Osterholm, Mark Olshaker and pay particular attention to the para’ that begins:

“What eventually stopped the spread was not high-tech medicine, since there wasn’t any specific treatment for SARS…

but really start reading from the previous page from “By April, the CDC and Canada’s National Microbiology Laboratory”

the above being in the chapter ‘SARS and MERS: Harbingers of Things to Come’ , which gives the lie to any claims that this came out of the blue, was unanticipated, unexpected.

Another useful section earlier in the book cited above begins:

“In some instances, the offending microbial agent is merely the trigger; the “bullet” comes from our own bodies…”

“In some instances, the offending microbial agent is merely the trigger; the “bullet” comes from our own bodies”

It should be noted that a Coronavirus patient may appear to be only slightly affected but a week or so into the illness becomes suddenly worse as the virus has replicated enough to cause a massive response from the immune system which overwhelms the lungs with debris (it is described as a burning of the lungs) causing organ failure through lack of oxygen – then death.

I am not sure what would happen to me personally for apart from having heart failure and consequent reduction of kidney function (due to lack of oxygen during the repeat myocardial infarctions over two days) I have something called MGUS (Monoclonal gammopathy of undetermined significance) which may make by immune system depressed or erratic.

Another useful source (even though it is mainly about the 1918 influenza outbreak it has material relevant to SARS) is The Great Influenza: The Epic Story of the Deadliest Plague in History by John M. Barry

IF the disease wasn’t communicable doggone it, not “it”.