by Heraclitusstudent ➕follow (8) 💰tip ignore
« First « Previous Comments 3,170 - 3,209 of 3,372 Next » Last » Search these comments
SARS-2 surges only in the winter, goes endemic after two waves, is impervious to vaccination, and has become harmless with Omicron
A brief look at the Corona pandemic in Europe from the perspective of excess mortality
A lot of the Corona data we’re fed is essentially meaningless propaganda, and it has obscured crucial patterns. Here, I want to look at the only metric that really matters, namely excess mortality, to make some basic points about what has happened to us since 2020, and what is happening now.
To date, the pandemicists have counted five or six waves of infection. If you ignore the case statistics, though, and look at nothing but European excess mortality, you see a totally different picture. Corona only has one deadly season a year, namely the winter, and no European country has seen more than two winter mortality spikes. ...
It’s definitely Omicron, and not the vaccines, that stopped the deaths. The same pattern exists in Austria, which is slightly less heavily vaccinated than Germany; and also in Hungary and Slovenia, which are substantially less vaccinated. ...
In Europe, Corona kills people for two seasons, and then it becomes a nothingburger, no worse than seasonal influenza in a bad year. You see exactly the same picture in England – two mortality waves, and then it’s over...
In most countries, the two-wave mortality surge was over by the time the vaccines were rolled out; in central Europe, it was still raging, but it was Omicron and not the vaccines that stopped the deaths.
has become harmless with Omicron
Towards a General Theory of Corona and Why No Interventions Ever Seem to Work As Intended
Why have lockdowns and other containment measures proven so generally ineffective against SARS-2? What causes waves of infection to begin, and why do they collapse long before all the susceptible have been infected? What is the significance of asymptomatic infection? Why do the vaccines seem to boost infections for a few weeks after the first and third doses? Why did the SARS-2 spike protein begin to experience heavy selection pressure in the latter half of 2020, giving rise to variants like Alpha and Delta? How did these variants manage so completely to replace prior lineages?
Increasingly, I wonder whether all of these questions aren’t just facets of the same phenomenon – one that was first described by R. Edgar Hope Simpson in his fascinating book on The Transmission of Epidemic Influenza (New York, 1992). As I said on Twitter, Hope-Simpson is one of the only people to have attempted what might be called a zoology of viruses. That is to say, he tried to analyse and explain how influenza interacted with its human hosts more broadly, and not just how it infected cells and responded to antibodies. This is precisely where modern epidemiology and virology are most deficient, with extremely simplistic understandings of how viruses behave across the population. ...
Hope-Simpson therefore concluded that influenza transmission was a far more subtle matter, than sick people infecting the healthy.
He proposed instead a two-phase process:
1) Acute infection, lasting a week or two, during which influenza is only transmitted very rarely.
2) Latency, whereby a subset of recovered people fail to clear the virus completely, and instead become asymptomatic carriers for many months, until seasonal factors correlated with latitude cause them to become infectious once again, generally without any noticeable recurrence of illness.
Alpha might have spread faster than wild-type SARS-2, but how did it actually succeed in wiping out these wild-type strains? Hope-Simpson calls this the “disappearing act,” as it is also observed with successive strains of influenza, and is very hard to account for.
Hope-Simpson finds the beginning of an answer in old influenza A antibody experiments:
During the great influenza A epidemic of the 1950–51 season, Isaacs in London, England and independently Archetti and Horsfall in the United States made a seminal observation. Two minor variants of the A (H1N1) subtype, “Scandinavian” and “Liverpool,” were co-circulating in many parts of the world. In both laboratories it was discovered that if the Scandinavian strain were made to infect a fertilized chicken egg in the presence of Scandinavian antibody, the strain harvested a few days later would turn out to be Liverpool. Vice versa, an appropriate dose of homologous antibody induced Liverpool virus-infected eggs to yield a harvest of Scandinavian virus.
The findings have been repeated with other strains of influenza virus in many laboratories throughout the world. (p. 99)
Some influenza strains, in other words, emerge spontaneously, via mutation, as a response or solution to the antibodies generated against other strains. Thus Hope-Simpson held that selection for new influenza strains happened primarily in the latent carriers of the virus, after acute infection.
Over months, the virus that lurked in carrier tissues was able to train itself against their immune response. Various mutant strains arose, and when the carriers became infectious again, the most contagious of these mutants went on to infect other people as the new influenza strain. Because the set of optimal solutions was in every case limited, all the latent carriers infected with the prior strain ended up incubating the same set of successor strains.
Booster will keep you protected for 6 weeks
The website cartoon shows three, if she wans't so lazy to investigate it.
The criteria above for the NYC Monkeypox vaccine would deny an under 18-year-old who was a victim of multiple abusers.
« First « Previous Comments 3,170 - 3,209 of 3,372 Next » Last » Search these comments
patrick.net
An Antidote to Corporate Media
1,258,093 comments by 15,013 users - Ceffer, goofus online now