"The Transmission of Epidemic Influenza - R. Edgar Hope-Simpson (1992)"

PDF: https://docdro.id/pRgxQQ8

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I certainly hope that the asymptomatic spread portion doesn't bear out. As ineffective as masking has been, if asymptomatic spread were proven then the pressure to "do something" by masking up would overwhelm all rationality and logic, and we would once again be forced to wear face diapers.

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Imagine. Living (or something-like-living) things behaving in complex interrelated ways.

I keep trying to tell you how much I enjoy these posts but never quite manage to encompass the full extent of it. You make scientific theories quite pleasurably interesting.

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Jun 26, 2022Liked by eugyppius

What if SARS-COV-2 wasn't at all novel. Recall the taxonomy committee did NOT agree with the WHO in naming this sas it did, it did not regard it as novel enough.

What if it was one of a continuum of mutating coronaviruses, moving in and out of zoonotic reservoirs. Sometimes causing colds, sometimes a "nasty bug"?

What if Omicron was just another one of these? It seems to be too different to "Wuhan" to be regarded as an evolutionary descendent.

What if we are now just measuring new waves of coronaviruses we never noticed before - possibly made somewhat worse by the interventions - inc vaccination.

What if the excess death curves were not related (except to a very small degree) with a virus but rather to the disruption to healthcare, combined with teerror and fear directed at populations.?

Why - if a supposedly lethal virus was spreading for months before - did excess death curves not shoot up UNITIL - rather than before - lockdowns?

What if the entire pandemic is actually an example of confirmation and observer bias - we are (through hysteria + PCR) shining a light on what we have never observed before in such detail.

This wouldn't be the first pseudo-pandemic fueled by PCR. But we need to make sure it's the last.

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"Virus gonna virus."

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The lack of any real noteworthy mutations except D614G for months is hard to explain, unless you assume that once we first learned of its existence it had already stumbled upon a strong local optimum for transmission in immunologically naive hosts. Such a thing can be explained if you assume the whole thing came into existence due to passage through mice with humanized ACE2 receptors. If we go with the competing "some dude ate a bat" model, the lack of genetic diversity observed is a lot stranger.

If the vaccine trials led to the emergence of these variants, that were generally more virulent and contagious and infected mostly naive people, then they were already responsible for millions of deaths before they ever received emergency use authorization.

"So why didn't the millions of naturally immune people we must have had by April 2020 or so give rise to variants early on in the pandemic? Why would it depend on the handful of early participants in the vaccination trials?" Would be the obvious question, but it could then presumably be explained through two factors:

1. The virus had already arrived at a strong local optimum during its birth in the Wuhan lab.

2. The spike directed vaccines impose the kind of selective pressure that asymptomatic lingering infections could overcome with select spike mutations, whereas in the naturally immune, the jumps that had to be taken on the fitness landscape to both escape the host's growing immune pressure AND give rise to new variants with a transmission advantage over Wuhan in naive hosts (ie most of the population) would simply have been too big.

A distorted immune response induced by the vaccines would have allowed the kind of changes to emerge that don't have a meaningful fitness advantage in naturally immune hosts. If all you really have to deal with as a virus are a lot of antibodies against your Spike protein, you may find that mutations that wouldn't have helped you out much if you were also dealing with T cells, a trained innate immune response etc hunting ALL of your proteins are suddenly quite useful. These mutations would now under these abnormal conditions be able to overcome whatever inherent structural disadvantage they may have that normally translates into a fitness disadvantage.

Some of those spike mutations in these variants suddenly under positive selective pressure would then have had pleiotropic effects, that enabled jumps into animal populations (see: N501Y, found in Beta and known to expand the range of viable hosts). In those animals the ACE2 protein looks different, along with the immune pressure, so new variants emerged and one of those variants jumped back into our species and thereby gave rise to Omicron, which proved to be sufficiently different to enable widespread reinfection.

Why does South Africa produce all these Omicron variants? If you follow this logic, you would consider they were early with the vaccine trials, so they were early with giving rise to variants with pleiotropic spike mutations and so their local wildlife has also had far more time to give rise to variants that can jump back into our species.

If you look at it this way, then it looks as if after the original lab accident, we could have had a Wuhan wave followed by genuine herd immunity, in the absence of any attempt to vaccinate against this virus, something which many epidemiologists had anticipated.

Considering these vaccines were ever approved to begin with, it's tempting to think our policymakers and the vaccine manufacturers assumed the virus was going to run into an evolutionary dead end too. They would have failed to consider that the vaccine trials themselves were expanding the range of viable positions on the fitness landscape, both directly and indirectly (through the new variants jumping into other species).

Corona viruses mutate at a fraction of the speed of Influenza viruses and if it could not have independently gone from Wuhan to Omicron without humans providing some of the intermediate stepping stones with the Spike based vaccine trials, then the present day situation where herd immunity is now definitively out of the question could be entirely our own fault.

But there would be other conclusions to draw too. The BA.1 spike vaccines now being deployed, experiments with nucleocapsid only vaccines, or vaccine trials that only carry the receptor binding domain as opposed to the whole spike protein in hopes of reducing side-effects, could once again give rise to unique selective pressures in certain hosts who would then be able to give rise to new variants that could not have come into existence otherwise.

We would have to consider that vaccinating people with just a portion of a pathogen is intrinsically dangerous, because it generates abnormal narrowly focused selective pressures in hosts. Today nobody really cares about that idea because it's assumed some immunocompromised people are the variant factories, even though such people will generally be hampered in their ability to deal with all SARS-COV-2 proteins and thus don't seem like good candidates to impose the type of oddly narrow selective pressures we're looking for.

TL;DR: If this is how it works, if the model in which healthy hosts can be variant factories under the right conditions is correct, the implications are massive and we may be responsible for millions of deaths ourselves through the vaccine trials.

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It's almost like it's really complicated with perhaps hundreds of variables we can't even identify.....

I'm just waiting for them to start blaming excessive human CO2 emissions for the viral mutants.

Stop Climate-Viral Change! I can already envision the retarded slogans and memes.

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So I understand correctly, one of the processes you seem to be theorizing may be at play with COVID is a phenomenon of POST-symptomatic transmission, not the pre-symptomatic/asymptomatic transmission theory used to create an unfalsifiable logic trap ("you can literally never prove or disprove that you cannot spread covid so we must assume everyone is a vector forever") that stole 2 years of our lives?

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Jun 26, 2022Liked by eugyppius

So basically, we might actually carry the proto-viruses or potential for infection around until opportunity arises for the virus. It also ties virology together with the more sane parts of terrain hypothesis, namely that external circumstances might trigger the virus to start breeding and causing an infectious outbreak in the host. Maybe our mothers were right when they said "Button your shirt or you'll get a cold, exposing your throat like that!"?

But how would one conduct a study to tst the hypothesis?

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There’s no good evidence for a novel virus causing mass illness. See work by Denis Rancourt & excellent interview on Jerm Warfare.

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Jun 26, 2022Liked by eugyppius

I observe a misunderstanding in the comments. Maybe I am wrong but his thesis states that some individuals would carry the bug asymptomatically, eventually getting SICK and then spreading it. That doesn't equate asymptomatic transmission.

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Jun 26, 2022Liked by eugyppius

'Our attempts to manage the pandemic have presented us with a variety of problems and paradoxes: Why have lockdowns and other containment measures [vaccines presumed included] proven so generally ineffective against SARS-2?'

Eugyppius, I am shocked – SHOCKED – that you could say such a thing. According to everybody's favorite infallible modelers at Imperial College London, the vaccines, at least, have done a stellar job. As we all know, models never lie.

'Covid-19 vaccines cut the potential global death toll by more than half in the first year they were available, according to a study published Thursday in The Lancet Infectious Diseases' https://www.statnews.com/2022/06/23/covid19-vaccines-prevention-global-deaths/

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Jun 26, 2022Liked by eugyppius

This fascinating review/update on Hope-Simpson's work was shared on Toby Young's Lockdown Sceptics site by @Nessimersion way back in Jan '21.

Key questions for the framing of a parsimonious explanation are asked that remain unanswered and the key role of VitD first came to my attention. It shows how little we know about this phenomenon, the things we call viruses and how much is a contingent construct.


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Jun 27, 2022Liked by eugyppius

Hope-Simpson's failure to identify a serial interval for influenza (where he had been able to do so for measles) seems to have been a turning point for him. He found no obvious pattern in the length time it took for household contacts of flu patients to become infected. I'm not sure how epidemiologists explain this away, but it seems to me a terribly important point. Can anyone explain it to me? If Person A, through close contact or proximity, transmits a disease to Person B, when we look at many pairs of household contacts, A and B, should be not see some pattern in the time between infections? Hope-Simpson argues, in effect, that without correlation there is no causation...he was right, wasn't he?

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The thing that made me angriest in the beginning of Covid was the notion that somehow asymptomatic people could be infectious, which is what I understand Hope-Simpson to be saying. This made everyone a potential disease vector and ramped up everyone’s fear.

If it turns out that asymptomatic people can be infectious, I just hope people will not go around avoiding each other bc of fear of potential illness.

Let us live! And if we’re actually sick, we’ll stay home.

All we need is hypochondriacs running the show. Dear God, no.

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Excellent and worth pursuing

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