Well, whatever the 1918 so-called "Spanish Flu" was, it was REAL whether lab-created or
natural! My dear grandfather caught it as a young man and was profoundly deaf for the rest of his life. He lived to be 90. I caught "the flu" at 9 in 1957 and afterwards almost died of pneumonia. However, since 2009 I have not had any flu at all including COVID-19 after being exposed to it. Why? In that year I read a leaked doctor's email telling someone to take NAC (Cysteine, an amino acid) 120 mg. a day to prevent H1N1 virus. (This doctor later denied writing this email. Yeah.) We started taking Swanson Vitamins' NAC 600 mg. capsules then and no more flu or shots either! About $10.00 a bottle. Child: 1/Day Adult: 2/Day This natural substance greatly helps the lungs, liver, and much of the body.
IT'S A WIN-WIN! A worse problem are the possibly bio-weapon quackcines!
SURVIVE AND STAY WELL NATURALLY! I post publicly and freely on MeWe.
Hm, not sure what interaction with LPS actually adds. Spike is amyloidogenic on its own. LPS is also amyloidogenic, but it's as common as household dust (it's in household dust). All viruses should be assumed to interact with the microbiotic molecular milieu in ways we can't possibly grasp. Polio virus seems to leverage some bacterial peptides, for example. This doesn't force us to redefine polio as some kind of virus-bacteria hybrid.
Where did the 1918 pathogenic agent come from? From China. The meteor showers which accompanied the passage of comet Halley in 1910, brought galloping tuberculosis to China.
I remember the claim of experiments having been made 1918, attempting to infect soldiers with flu, and it supposedly failed. Some people took that as "proof it was not flu that killed all those people".
Quick attempt a finding _something_ ... yielded this, it seems to describe roughly some of what I remember under the name "gallup island files" I was given.
I also remember the claim that the death ascribed to the flu had an atypical spreading pattern for such a thing, remember no details. IIRC the book" Virus Mania" supposedly has it, I don't have the book.
At least one of the authors is, if I'm not mistaken, one of the "no viruses" folks, but not all of them. Köhnlein is an internist by profession, I remember him as seeming measured.
Shope also reviews the fiasco of contemporary challenge trials, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1951634/ - of course, he is also the source for the strongest evidence that 1918 influenza-like illness is related to the virus. Namely, that pigs in the midwest started getting flu-symptoms that late summer and every year after, but human blood samples stop protecting lab animals from the 1930/1 swine strains in people born after ~1923. So pigs had basically kept a record of the 1918 version of the virus alive.
Aug 23, 2022·edited Aug 23, 2022Liked by Brian Mowrey
One interesting point here is that apparently the reintroduced 1957 H1N1, had no issues competing with its own descendant H3N2 despite the latter having years of mutational opportunities. That seems to underline indeed that herd/population immunity is what is driving infections, and not so much evolutionary improvements.
And that also explains why variants come and go for decades. They go once they do not succeed in mutating fast enough to evade population immunity. Then they jump back from animals decades later once the population is naive again.
What seems puzzling then is, why H1N1 did not die out in its animal reservoir. Is it simply short lifespan and hence the high reproduction rate of birds that allows for a continuous fresh naive population, requiring no evolutionary pressure? That seems reasonable, but would also let me believe that COVID will then die out. It has no animal reservoir that we know of, and there is no reason to believe it is mutating as fast as flu (*) or somehow our immune system will fail to protect against Omicron-variants in ways less than it does for flu-strains.
*) on the contrary it seems. If it wasn't for the Omicron savior, it would have looked dim. Delta appeared in 2020 and no new dominant variant appeared for a year. The best it could muster up while infecting over a billion people was the 4Y mutation with ~10% higher infectiousness. All while prior infection topped 90% protection consistently. The jury is still somewhat out if prior-Omicron protects against future-Omicron, but my bet would be that it does *enough* to push its R value below one. If so it will be game over eventually. So unless it somehow manages to dramatically up its game in terms of mutations, or gets animal reservoirs, our children may look at this period in time even more bewilderment than we do.
I agree with your assessment on Wuhan to Delta not being impressive in terms of antigenic escape. This is why I am open to the idea that even B.1 and Delta are separate lab creations, because neither displayed dynamic tendencies in the wild. Omicron just continues and magnifies this suspicious "staccato evolution" trend.
Fowl are super-permissive of influenza A; it has been isolated from them 1000s of times from asymptomatic birds. So the circulating species of HA genes, including H1, are never in much danger of dying out. And nor are they subject to any immune pressure; for this reason, even their receptor binding regions are highly conserved to favor the most intrinsically fitness-conferring design rather than novelty. Fowl and influenza A may be co-evolved at this point so that birds rely on flu to "prune" the upper layers of their GI epithelium; maybe this helps recycle nutrients to allow for faster regeneration and healing for all the hard stuff they end up with in their stomach, who knows.
Nitpick: You say B.1 and Delta separate lab creations. I assume you mean BA.1 (Omicron) vs Delta, right?
This as B.1 was the Italian outbreak variant, which has the key D416G mutation compared to the Wuhan/WIV-lab strain. All other variants after that evolve from that, including Delta (aka B.1.617.2). So from B.1 to B.1.617.2 (Delta) there are (surprisingly) little successful mutations aimed at immunity escape, and even few optimization mutations like 4Y considering the length of Delta's reign.
But yes, if I did not misunderstand you, then I agree, the BA.1/2 pair is likely a 2nd lab creation. I do think it is then a more a smaller 'oops' as in vaccine or other post-outbreak research based on an already pandemic B.1. So not in the same sports league as taking a non-Human virus and adapting it to cause the death of a few million people.
One further point I just realized is that the fact that Omicron outcompeted Delta, seems to me indicate that Omicron immunity does protect (enough) against Delta. Else Delta would just have stayed on as well.
I say this as with H1N1 vs H3N2 that question is somewhat open. It is possible that immunity against H3N2 is (partially) cross-protective against H1N1, but their relative infectiousness is balanced enough so neither one ever wins out considering both keep mutating fast enough too.
But with Omicron against Delta, this is no real contest, and if Omicron immunity would NOT protect (enough) against Delta, you'd just see them co-exist.
And finally, the idea that flu and birds may co-evolved is intriguing. I need to read up on that. That would be another reason why stability would be preferred from evolutionary point. Either way, thank you for the educational article. I learned several things!
B.1 refers to a triplet of mutations which appeared near-simultaneously in many part of the world in February and March 2020 - Spike D614G, Orf1 P4715L, and the silent c3037u - this constitutes a "signature" which doesn't become fixed until the VOCs arrive in late 2020. So it's suspicious that no D614G's without the signature were similarly durable simply via convergent evolution. It's also suspicious that Wuhan isolates later subjected to mouse passage don't produce any B.1 triplet mutations, but the Omicron LCA (BA.0 in my system) shows signs of mouse passage; but it has the B.1 triplet - in other words, the BA.0/Wuhan LCA is *literally* B.1 (no other common early 2020 mutations). So B.1 is probably a lab stock virus. This theory of mine was debuted here but needs its own post one day https://unglossed.substack.com/i/49133098/-it-wasnt-after-wuhan
As for the co-fixation of H3N2 and H1N1 after 1977, my hunch would be that they have enjoyed a synergistic relationship where cross-interference makes it take longer for either to "burn out" in terms of physically/mutationally possible variants. It could be that this yin-yang synergy was always a possible, but clonal interference from the current strain was too binary (on = prevent crossover / off = die out easily) without a swine / lab reservoir of a near-human or human-adapted alternate HA model.
Why is it suspicious? The D614G has an enormous benefit, perhaps not alone but needed the other two, but either way concurred the world quickly once introduced. In 2020 the "consensus" was this originated in Southern Germany or Nothern Italy. I have no strong opinion here, and the fact that these mutations naturally evolve in other places makes this perhaps hard to judge. But just as the numeric center of Wuhan/WIV-lab strain was clearly in Wuhan, the numeric center seems to strongly suggest B.1 originated from Europe. Or at least it originated its spread from there.
But let's say I'm wrong. There seems to be still no Occam's Razor need to suggest B.1 is a lab-stock. B.1 seems to be capable of naturally have evolved from Wuhan/WIV-lab. We only make the mystery larger, as one now has to explain WIV-lab release dating back to let's say October 2019, B.1 stock appearance in February 2020 and the BA.0 evolution and release in November 2022. We go from 2 to 3 mysteries.
I do agree that the fact that Wuhan isolates subjected to mouse passage don't produce any B.1 triplet mutations, but Omicron does seem to have signs of mouse passage is interesting. It seems to suggest that the jump-to-mouse and back-to-humans as a means to explain its mutational route using a natural animal reservoir, is less likely. But I was not sold on that single study anyway. Plus it was written when BA.2 wasn't mainstream yet. The arrival of BA.2 makes the natural mouse-route unlikely anyway, as it would not necessarily explain the difference in mutational direction between BA.1 and BA.2, and make it odd they just happen to both jump back at the same time.
I may miss your point, but whether B.1 is lab-stock, only becomes important if one wants to insist BA.0 is not derived from natural (Italian) B.1, but derived from an unrelated WIV stock that just happens to look like B.1 because these mutations were likely to appear anyway. Unless I miss your point, that would pretty much mean that it was somehow (deliberately?) released in November 2021 again by Chinese.
But that seems pure speculation, and not inherently more or less likely compared to the alternative that someone grabbed some natural B.1 and experimented for 1.5 years, before we had our second 'oops'. We've had hundreds of laboratories initiated experiments in the early 2020's.
The key question seems to be either way, why BA.0 evolved outside the wild from either natural of lab-stock B.1 and then split into BA.1/2 and continued with heavy non-symmetric pressure and then was released. At this point it seems to be that has to be a lab-leak (or lab-release) regardless of which B.1 we base BA.0 on.
Or did I manage to completely miss your point? :-)
This is the most plausible alternative, yes - that someone plucked B.1 out of early circulation because of observed performance.
But once the most plausible alternative has a giant human footprint in it, you have to reinterpret the other evidence in light of theory of mind for whoever left the footprint. In other words, you have to keep in mind that a person who would pluck B.1 out of circulation was also around before B.1 - so it’s obviously possible the same entity also made B.1.
Thus, in the case of the geographically decentralized emergence of the B.1 triplet, Occam’s Razor is scores natural evolution harshly, since B.1 would somehow have to have been seeded everywhere around the world before emerging from the “swarm” in any sequences, and scores “B.1 rescuer is actually B.1 creator” not too harshly.
RE the latter, besides the mouse passage argument for nonexistence of B.1 in the “swarm,” I now find the logistics implausible without artificial intervention (because dispersion / dilution should enforce consensus, reducing the chances for “goldilocks” variants in the swarm to travel until *after* they make a foothold in one location). Meanwhile, it’s not impossible that all three mutations are independently or co-entropic from Wuhan, making triple-convergent evolution possible after Wuhan seeded the globe, but it seems unlikely as far as c3037u. That is a very non-meaningful swap even in terms of RNA secondary structures and so it says “signature.”
Oh, I would imagine the US as the more likely steward of the B.1 “stock” than China.
I'm not sure if I agree with the B.1 triplet theory though. D614G seems to have rapidly expanded on its own and became dominant before fall. Perhaps it needed synergy with Orf1 P4715L, though. I haven't looked at that, so perhaps I'm just misremembering. Either way interesting.
On C3037U, I believed that is a homoplasy? Or in other words, just a biochemical preference and had occurred many times before. E.g. [https://www.nature.com/articles/s41467-020-19818-2.pdf] suggested that it was just pressure due to the immune system (or alternatively just being in actual humans vs cell cultures) that caused these mutations to dominate.
Often it is forgotten that mutations don't have to be beneficial to be frequent and eventually dominate. If the biochemical environment favors it, it will happen often, and potentially even against evolutionary pressure. It is in fact expected that once jumping a specie such changes will happen sooner than later. (Monkeypox saw a similar behavior now we have human-to-human vs rodents-to-human, and hence the African outbreak is a different strain than the US/European.)
To be fair, I have not considered your swarm enough though. So something for me to digest, as I also cannot refute it either I admit.
I still find it a side-argument though. Does it really matter whether B.1 was always there in the swarm and emerged due to being better adapted to actual humans vs lab-cells, or as I still think, naturally evolved from the Wuhan/WIV strain? Neither of this inherently explains why/where BA.0 evolved, and why the split into BA.1/2 and simultaneous release.
This is so much science here it makes me hope that we get back to a place where that matters more widely in public discussion, thanks for the incredible effort. Since you mentioned you're open to the bacteria theories and my earlier reply to a user comment has a link to Rockefeller Institute vaccine experiments that rolled out to the military recruits. Mathew Crawford's Campfire wiki has a nice assortment of seldom seen links for Spanish Flu and Swine Flu worth scanning for hidden gems. :~)
Thank you - and for the 1917 paper below, that was an interesting one.
The best counter-argument to the bacteria vaccine theory (much like the aspirin theory) is the alleged high death counts in tropical and remote areas. But, validating those would require trying to rebuild the data chain of custody for western counts of remote public health figures. The most reliable source might be India, which had a functional bureaucracy, but also had a vaccine lab...
Not the stats you mentioned but happy coincidence crossing my radar now.. lots of leg work on the bacteria theory, including Fauci authored investigation w autopsies that may be handy.
In my early years I was intimately familiar with the flu. In 1957 at nine I almost died of double pneumonia after having it. (Also a bad year for it.) My grandfather had lost most of his hearing from
the influenza as a young man in 1918. (And he lived until 90!) In 2009 there was a Web rumor from a leaked doctor's email. He stated that taking 120 mg. of NAC (Cysteine, an amino acid) daily will prevent H1N1 virus. We started taking Swanson Vitamin's NAC 600 mg. capsules in the winter time. We both did not have any flu or Coronavirus again or vaccines either. I was directly exposed to COVID-19 in January, 2020 and did not suffer any symtoms. Yay! Years ago I started taking it full time as NAC is very good for the lungs, liver, and whole body. It's about $10.00 a bottle. Child: 1/Daily Adult: 2/Daily
I post publicly on MeWe after being kicked off of Facebook and Twitter. STAY WELL NATURALLY!
ETERNAL LIFE BLESSINGS FOR YAHWEH'S SAINTS! HalleluYah! Hebrew: "Praise ye Yah!"
I’m definitely not a scientist or doctor, but several years ago, I read an article about how the overuse of aspirin during the 1918 flu pandemic could have contributed to so many deaths.
Thank you - definitely worth taking a look at. Another parallel is the question of how often penicillin injections were administered to kids showing general infection symptoms in polio season, and if this could have bypassed mucosal immunity in the gut and delivered the virus to the blood. But it’s hard to find raw numbers.
This counter-argument buys into a lot of the probably exaggerated modern death counts, but still makes a good case - https://academic.oup.com/cid/article/50/8/1203/451446 - as mentioned in my footnotes the alleged mortality in tropical areas is also why I dismissed my own “hygiene hypothesis” account for the observed death rate.
Have you seen the theory that the reason so many young fit people died in 1918 is because they were given a vaccine - can’t remember the details but think it involved horses and encephalitis or meningitis. I expect you could find a video on it on bitchute or brand new tube etc?
Pretty sure you are confusing two different stories if illness and sources. First and very plausible is that animals shipped across the Atlantic Ocean along with troops in close quarters with illness and death contributed to sickness in the soldiers that spread as they traveled to Europe and back. Nice history of animal transport conditions without human health issues.
"Newport News was the principal port for exporting horses and mules from the USA and when the USA entered the war, it built there a 77-acre complex of pens and stalls to provide for their own expeditionary force, shipping nearly 50,000 animals in under a year.
Once on board the ships, the animals were placed in their stalls and given regular checks throughout the voyage. Despite the best efforts of the men who looked after them, many horses suffered from 'shipping fever', a form of pneumonia, and from various pulmonary complaints.
After their confinement, horses usually required several weeks to recuperate on landing. It was the job of the Remount Department and the Army Veterinary Corps to get them into shape and ready for active service.
The vaccines story is better documented as far as connection to human health and important consideration. In preparation for WW1, a massive military vaccination experiment involving numerous prior developed vaccines took place in Fort Riley, Kansas- where the first “Spanish Flu” case was reported. Two great reference links for that so the Rockefeller vaccine experiments can be verified.
Original study - A R E P O R T ON A N T I M E N I N G I T I S VACCINATION AND
OBSERVATIONS ON AGGLUTININS IN T H E BLOOD OF CHRONIC MENINGOCOCCUS CARRIERS.
BY FREDERICK L. GATES, M. D. - First Lieutenant, Medical Corps, U. S. Army.
(From the Base Hospital, Fort Riley, Kansas, and The Rockefeller Institute ./or
Medical Research, New York.) (Received for publication, July 20, 1918.)
I doubt they were truly fit; the 10’s were an era of widespread tininess. A lot of photos of soldiers in WWI are startling in this regard.
More to the point, Shope makes a case that memory immunity from the spring wave was protective in the autumn wave https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1951634/ , p 174 (although this has been debated both before and since). Memory immunity protection would not be observed if deaths in the autumn wave were caused by secret bacteria vaccine trials. So, make of the case for memory immunity what you will. It’s obviously a messy story with a lot of emotion and little precision.
Brian, Is "OAS" = "Original Antigenic Sin"? It would be helpful if you fully texted your acronym before you use it. "OAS" could be "Organization of American States"; obviously not in your context. Only selecting footnotes 14 & 17 and learning about "OAS", and not "OAS", was I able to make better sense of your writing. Also, it may appeal to the non-experts to read further. Thank you for writing an eye opening "T" = thesis.
Thank you, I will fix it when I have a chance. There was a lot of editing-down of the introduction as this post was initially going to be framed in terms of my larger series, on Optional Airborne Salamanders. So the specification of the acronym was dropped by mistake. It definitely refers to Orthogonal Attic Structures.
A better question would be "why spend any time on the statements of scientists when they are part of the eugenicist's agenda"? Why believe anything they say at all? Their first allegiance is to their paycheck. Why even care about what they say let alone research it and make a case against it? All of science is spell magik. It diverts us from the truth. Why are possible other causes not aired or not even mentioned? Causes like electromagnetic radiation that is making people sick? You didn't mention anything about 5G and it's rollout over the last two years which has been at a heavy clip done behind our backs and in silence. The symptoms of electromagnetic radiation probably poisoned the people in 1918 with the world wide roll out of electricity. It's amazing to me that things that are staring us in the face are never mentioned. Like the deaths from the vaccines. It's like doctors now can't put two and two together all because of that confounded paycheck.
Two of my former colleagues published this about 10 years ago, which is also relevant to reconsideration of the threat from the Great Influenza:
"Of the unexplained characteristics of the 1918–19 influenza pandemic, the extreme mortality rate among young adults (W-shaped mortality curve) is the foremost. Lack of a coherent explanation of this and other epidemiologic and clinical manifestations of the pandemic contributes to uncertainty in preparing for future pandemics. Contemporaneous records suggest that immunopathologic responses were a critical determinant of the high mortality rate among young adults and other high-risk subgroups. Historical records and findings from laboratory animal studies suggest that persons who were exposed to influenza once before 1918 (e.g., A/H3Nx 1890 pandemic strain) were likely to have dysregulated, pathologic cellular immune responses to infections with the A/H1N1 1918 pandemic strain. The immunopathologic effects transiently increased susceptibility to ultimately lethal secondary bacterial pneumonia. The extreme mortality rate associated with the 1918–19 pandemic is unlikely to recur naturally. However, T-cell–mediated immunopathologic effects should be carefully monitored in developing and using universal influenza vaccines."
The part about susceptibility to unfamiliar everyday bacteria due to movement is an interesting candidate for a non-repeated environmental cofactor. The whole thing still seems a tiny bit shaky as far as the high death rates in remote or tropical areas and young adult mortality not repeating in 1958 and 1968. I will add a consideration of this in the appendix, whereas without these papers I wasn't going to take the immune overreaction theory into consideration to begin with - thanks
"Deaths during the 1918–19 influenza pandemic have been attributed to a hypervirulent influenza strain. Hence, preparations for the next pandemic focus almost exclusively on vaccine prevention and antiviral treatment for infections with a novel influenza strain. However, we hypothesize that infections with the pandemic strain generally caused self-limited (rarely fatal) illnesses that enabled colonizing strains of bacteria to produce highly lethal pneumonias. This sequential- infection hypothesis is consistent with characteristics of the 1918–19 pandemic, contemporaneous expert opinion, and current knowledge regarding the pathophysiologic effects of influenza viruses and their interactions with respiratory bacteria. This hypothesis suggests opportunities for prevention and treatment during the next pandemic (e.g., with bacterial vaccines and antimicrobial drugs), particularly if a pandemic strain–specific vaccine is unavailable or inaccessible to isolated, crowded, or medically underserved populations."
Thank you - this is stronger support for the secondary bacteria infection etiology than I was aware existed, especially the sources for Figure 1. That helps since as my footnote mentions I was a bit hesitant to buy into the evidence for that one.
Well, whatever the 1918 so-called "Spanish Flu" was, it was REAL whether lab-created or
natural! My dear grandfather caught it as a young man and was profoundly deaf for the rest of his life. He lived to be 90. I caught "the flu" at 9 in 1957 and afterwards almost died of pneumonia. However, since 2009 I have not had any flu at all including COVID-19 after being exposed to it. Why? In that year I read a leaked doctor's email telling someone to take NAC (Cysteine, an amino acid) 120 mg. a day to prevent H1N1 virus. (This doctor later denied writing this email. Yeah.) We started taking Swanson Vitamins' NAC 600 mg. capsules then and no more flu or shots either! About $10.00 a bottle. Child: 1/Day Adult: 2/Day This natural substance greatly helps the lungs, liver, and much of the body.
IT'S A WIN-WIN! A worse problem are the possibly bio-weapon quackcines!
SURVIVE AND STAY WELL NATURALLY! I post publicly and freely on MeWe.
ETERNAL LIFE BLESSINGS FOR YAHWEH'S SAINTS!
I wonder if you have seen this article. Parts of it are a little over my head, but I get the point that it is bad.
https://hiddencomplexity.substack.com/p/sars-cov-2-spike-aggregation-and?utm_source=substack&utm_medium=email
Hm, not sure what interaction with LPS actually adds. Spike is amyloidogenic on its own. LPS is also amyloidogenic, but it's as common as household dust (it's in household dust). All viruses should be assumed to interact with the microbiotic molecular milieu in ways we can't possibly grasp. Polio virus seems to leverage some bacterial peptides, for example. This doesn't force us to redefine polio as some kind of virus-bacteria hybrid.
1915-1917 M. avium pandemic (described as "coronavirus")
https://academic.oup.com/jtm/advance-article/doi/10.1093/jtm/taaa206/5955501
1918 M. influenzae/M. africanum/M. tuberculosis (galloping tuberculosis)
https://scientiaricerca.com/srprrc/SRPRRC-01-00011.php (explains that H1N1 was actually Haeomophilus influenzae)
Where did the 1918 pathogenic agent come from? From China. The meteor showers which accompanied the passage of comet Halley in 1910, brought galloping tuberculosis to China.
https://www.gjenvick.com/Influenza/IsTheInfluenzaAChinesePlague-1918-12.html
The catalyst for the 1918 M. influenzae pandemic was: 1. the toxic doses of aspirin 2. the eruption of the Katla volcano (12 October 1918).
2019-2021 M. avium (Sars-Cov-2)
2022 M. influenzae (aka Mers-Cov/Omicron)
This is some impressive research, thanks so much! 👍🏽💕
I remember the claim of experiments having been made 1918, attempting to infect soldiers with flu, and it supposedly failed. Some people took that as "proof it was not flu that killed all those people".
Quick attempt a finding _something_ ... yielded this, it seems to describe roughly some of what I remember under the name "gallup island files" I was given.
https://www.gjenvick.com/Influenza/TheRosenauExperiment-1918-1919.html
Not sure was this really means ;)
I also remember the claim that the death ascribed to the flu had an atypical spreading pattern for such a thing, remember no details. IIRC the book" Virus Mania" supposedly has it, I don't have the book.
At least one of the authors is, if I'm not mistaken, one of the "no viruses" folks, but not all of them. Köhnlein is an internist by profession, I remember him as seeming measured.
Shope also reviews the fiasco of contemporary challenge trials, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1951634/ - of course, he is also the source for the strongest evidence that 1918 influenza-like illness is related to the virus. Namely, that pigs in the midwest started getting flu-symptoms that late summer and every year after, but human blood samples stop protecting lab animals from the 1930/1 swine strains in people born after ~1923. So pigs had basically kept a record of the 1918 version of the virus alive.
One interesting point here is that apparently the reintroduced 1957 H1N1, had no issues competing with its own descendant H3N2 despite the latter having years of mutational opportunities. That seems to underline indeed that herd/population immunity is what is driving infections, and not so much evolutionary improvements.
And that also explains why variants come and go for decades. They go once they do not succeed in mutating fast enough to evade population immunity. Then they jump back from animals decades later once the population is naive again.
What seems puzzling then is, why H1N1 did not die out in its animal reservoir. Is it simply short lifespan and hence the high reproduction rate of birds that allows for a continuous fresh naive population, requiring no evolutionary pressure? That seems reasonable, but would also let me believe that COVID will then die out. It has no animal reservoir that we know of, and there is no reason to believe it is mutating as fast as flu (*) or somehow our immune system will fail to protect against Omicron-variants in ways less than it does for flu-strains.
*) on the contrary it seems. If it wasn't for the Omicron savior, it would have looked dim. Delta appeared in 2020 and no new dominant variant appeared for a year. The best it could muster up while infecting over a billion people was the 4Y mutation with ~10% higher infectiousness. All while prior infection topped 90% protection consistently. The jury is still somewhat out if prior-Omicron protects against future-Omicron, but my bet would be that it does *enough* to push its R value below one. If so it will be game over eventually. So unless it somehow manages to dramatically up its game in terms of mutations, or gets animal reservoirs, our children may look at this period in time even more bewilderment than we do.
I agree with your assessment on Wuhan to Delta not being impressive in terms of antigenic escape. This is why I am open to the idea that even B.1 and Delta are separate lab creations, because neither displayed dynamic tendencies in the wild. Omicron just continues and magnifies this suspicious "staccato evolution" trend.
Fowl are super-permissive of influenza A; it has been isolated from them 1000s of times from asymptomatic birds. So the circulating species of HA genes, including H1, are never in much danger of dying out. And nor are they subject to any immune pressure; for this reason, even their receptor binding regions are highly conserved to favor the most intrinsically fitness-conferring design rather than novelty. Fowl and influenza A may be co-evolved at this point so that birds rely on flu to "prune" the upper layers of their GI epithelium; maybe this helps recycle nutrients to allow for faster regeneration and healing for all the hard stuff they end up with in their stomach, who knows.
Nitpick: You say B.1 and Delta separate lab creations. I assume you mean BA.1 (Omicron) vs Delta, right?
This as B.1 was the Italian outbreak variant, which has the key D416G mutation compared to the Wuhan/WIV-lab strain. All other variants after that evolve from that, including Delta (aka B.1.617.2). So from B.1 to B.1.617.2 (Delta) there are (surprisingly) little successful mutations aimed at immunity escape, and even few optimization mutations like 4Y considering the length of Delta's reign.
But yes, if I did not misunderstand you, then I agree, the BA.1/2 pair is likely a 2nd lab creation. I do think it is then a more a smaller 'oops' as in vaccine or other post-outbreak research based on an already pandemic B.1. So not in the same sports league as taking a non-Human virus and adapting it to cause the death of a few million people.
One further point I just realized is that the fact that Omicron outcompeted Delta, seems to me indicate that Omicron immunity does protect (enough) against Delta. Else Delta would just have stayed on as well.
I say this as with H1N1 vs H3N2 that question is somewhat open. It is possible that immunity against H3N2 is (partially) cross-protective against H1N1, but their relative infectiousness is balanced enough so neither one ever wins out considering both keep mutating fast enough too.
But with Omicron against Delta, this is no real contest, and if Omicron immunity would NOT protect (enough) against Delta, you'd just see them co-exist.
And finally, the idea that flu and birds may co-evolved is intriguing. I need to read up on that. That would be another reason why stability would be preferred from evolutionary point. Either way, thank you for the educational article. I learned several things!
B.1 refers to a triplet of mutations which appeared near-simultaneously in many part of the world in February and March 2020 - Spike D614G, Orf1 P4715L, and the silent c3037u - this constitutes a "signature" which doesn't become fixed until the VOCs arrive in late 2020. So it's suspicious that no D614G's without the signature were similarly durable simply via convergent evolution. It's also suspicious that Wuhan isolates later subjected to mouse passage don't produce any B.1 triplet mutations, but the Omicron LCA (BA.0 in my system) shows signs of mouse passage; but it has the B.1 triplet - in other words, the BA.0/Wuhan LCA is *literally* B.1 (no other common early 2020 mutations). So B.1 is probably a lab stock virus. This theory of mine was debuted here but needs its own post one day https://unglossed.substack.com/i/49133098/-it-wasnt-after-wuhan
As for the co-fixation of H3N2 and H1N1 after 1977, my hunch would be that they have enjoyed a synergistic relationship where cross-interference makes it take longer for either to "burn out" in terms of physically/mutationally possible variants. It could be that this yin-yang synergy was always a possible, but clonal interference from the current strain was too binary (on = prevent crossover / off = die out easily) without a swine / lab reservoir of a near-human or human-adapted alternate HA model.
Why is it suspicious? The D614G has an enormous benefit, perhaps not alone but needed the other two, but either way concurred the world quickly once introduced. In 2020 the "consensus" was this originated in Southern Germany or Nothern Italy. I have no strong opinion here, and the fact that these mutations naturally evolve in other places makes this perhaps hard to judge. But just as the numeric center of Wuhan/WIV-lab strain was clearly in Wuhan, the numeric center seems to strongly suggest B.1 originated from Europe. Or at least it originated its spread from there.
But let's say I'm wrong. There seems to be still no Occam's Razor need to suggest B.1 is a lab-stock. B.1 seems to be capable of naturally have evolved from Wuhan/WIV-lab. We only make the mystery larger, as one now has to explain WIV-lab release dating back to let's say October 2019, B.1 stock appearance in February 2020 and the BA.0 evolution and release in November 2022. We go from 2 to 3 mysteries.
I do agree that the fact that Wuhan isolates subjected to mouse passage don't produce any B.1 triplet mutations, but Omicron does seem to have signs of mouse passage is interesting. It seems to suggest that the jump-to-mouse and back-to-humans as a means to explain its mutational route using a natural animal reservoir, is less likely. But I was not sold on that single study anyway. Plus it was written when BA.2 wasn't mainstream yet. The arrival of BA.2 makes the natural mouse-route unlikely anyway, as it would not necessarily explain the difference in mutational direction between BA.1 and BA.2, and make it odd they just happen to both jump back at the same time.
I may miss your point, but whether B.1 is lab-stock, only becomes important if one wants to insist BA.0 is not derived from natural (Italian) B.1, but derived from an unrelated WIV stock that just happens to look like B.1 because these mutations were likely to appear anyway. Unless I miss your point, that would pretty much mean that it was somehow (deliberately?) released in November 2021 again by Chinese.
But that seems pure speculation, and not inherently more or less likely compared to the alternative that someone grabbed some natural B.1 and experimented for 1.5 years, before we had our second 'oops'. We've had hundreds of laboratories initiated experiments in the early 2020's.
The key question seems to be either way, why BA.0 evolved outside the wild from either natural of lab-stock B.1 and then split into BA.1/2 and continued with heavy non-symmetric pressure and then was released. At this point it seems to be that has to be a lab-leak (or lab-release) regardless of which B.1 we base BA.0 on.
Or did I manage to completely miss your point? :-)
This is the most plausible alternative, yes - that someone plucked B.1 out of early circulation because of observed performance.
But once the most plausible alternative has a giant human footprint in it, you have to reinterpret the other evidence in light of theory of mind for whoever left the footprint. In other words, you have to keep in mind that a person who would pluck B.1 out of circulation was also around before B.1 - so it’s obviously possible the same entity also made B.1.
Thus, in the case of the geographically decentralized emergence of the B.1 triplet, Occam’s Razor is scores natural evolution harshly, since B.1 would somehow have to have been seeded everywhere around the world before emerging from the “swarm” in any sequences, and scores “B.1 rescuer is actually B.1 creator” not too harshly.
RE the latter, besides the mouse passage argument for nonexistence of B.1 in the “swarm,” I now find the logistics implausible without artificial intervention (because dispersion / dilution should enforce consensus, reducing the chances for “goldilocks” variants in the swarm to travel until *after* they make a foothold in one location). Meanwhile, it’s not impossible that all three mutations are independently or co-entropic from Wuhan, making triple-convergent evolution possible after Wuhan seeded the globe, but it seems unlikely as far as c3037u. That is a very non-meaningful swap even in terms of RNA secondary structures and so it says “signature.”
Oh, I would imagine the US as the more likely steward of the B.1 “stock” than China.
Got it.
I'm not sure if I agree with the B.1 triplet theory though. D614G seems to have rapidly expanded on its own and became dominant before fall. Perhaps it needed synergy with Orf1 P4715L, though. I haven't looked at that, so perhaps I'm just misremembering. Either way interesting.
On C3037U, I believed that is a homoplasy? Or in other words, just a biochemical preference and had occurred many times before. E.g. [https://www.nature.com/articles/s41467-020-19818-2.pdf] suggested that it was just pressure due to the immune system (or alternatively just being in actual humans vs cell cultures) that caused these mutations to dominate.
Often it is forgotten that mutations don't have to be beneficial to be frequent and eventually dominate. If the biochemical environment favors it, it will happen often, and potentially even against evolutionary pressure. It is in fact expected that once jumping a specie such changes will happen sooner than later. (Monkeypox saw a similar behavior now we have human-to-human vs rodents-to-human, and hence the African outbreak is a different strain than the US/European.)
To be fair, I have not considered your swarm enough though. So something for me to digest, as I also cannot refute it either I admit.
I still find it a side-argument though. Does it really matter whether B.1 was always there in the swarm and emerged due to being better adapted to actual humans vs lab-cells, or as I still think, naturally evolved from the Wuhan/WIV strain? Neither of this inherently explains why/where BA.0 evolved, and why the split into BA.1/2 and simultaneous release.
This is so much science here it makes me hope that we get back to a place where that matters more widely in public discussion, thanks for the incredible effort. Since you mentioned you're open to the bacteria theories and my earlier reply to a user comment has a link to Rockefeller Institute vaccine experiments that rolled out to the military recruits. Mathew Crawford's Campfire wiki has a nice assortment of seldom seen links for Spanish Flu and Swine Flu worth scanning for hidden gems. :~)
https://www.campfire.wiki/doku.php?id=spanish_flu
https://www.campfire.wiki/doku.php?id=swine_flu
Thank you - and for the 1917 paper below, that was an interesting one.
The best counter-argument to the bacteria vaccine theory (much like the aspirin theory) is the alleged high death counts in tropical and remote areas. But, validating those would require trying to rebuild the data chain of custody for western counts of remote public health figures. The most reliable source might be India, which had a functional bureaucracy, but also had a vaccine lab...
Not the stats you mentioned but happy coincidence crossing my radar now.. lots of leg work on the bacteria theory, including Fauci authored investigation w autopsies that may be handy.
https://manuherold.substack.com/p/bad-bad-virus-passionate-grandpa
In my early years I was intimately familiar with the flu. In 1957 at nine I almost died of double pneumonia after having it. (Also a bad year for it.) My grandfather had lost most of his hearing from
the influenza as a young man in 1918. (And he lived until 90!) In 2009 there was a Web rumor from a leaked doctor's email. He stated that taking 120 mg. of NAC (Cysteine, an amino acid) daily will prevent H1N1 virus. We started taking Swanson Vitamin's NAC 600 mg. capsules in the winter time. We both did not have any flu or Coronavirus again or vaccines either. I was directly exposed to COVID-19 in January, 2020 and did not suffer any symtoms. Yay! Years ago I started taking it full time as NAC is very good for the lungs, liver, and whole body. It's about $10.00 a bottle. Child: 1/Daily Adult: 2/Daily
I post publicly on MeWe after being kicked off of Facebook and Twitter. STAY WELL NATURALLY!
ETERNAL LIFE BLESSINGS FOR YAHWEH'S SAINTS! HalleluYah! Hebrew: "Praise ye Yah!"
I’m definitely not a scientist or doctor, but several years ago, I read an article about how the overuse of aspirin during the 1918 flu pandemic could have contributed to so many deaths.
https://www.sciencedaily.com/releases/2009/10/091002132346.htm
Thank you - definitely worth taking a look at. Another parallel is the question of how often penicillin injections were administered to kids showing general infection symptoms in polio season, and if this could have bypassed mucosal immunity in the gut and delivered the virus to the blood. But it’s hard to find raw numbers.
This counter-argument buys into a lot of the probably exaggerated modern death counts, but still makes a good case - https://academic.oup.com/cid/article/50/8/1203/451446 - as mentioned in my footnotes the alleged mortality in tropical areas is also why I dismissed my own “hygiene hypothesis” account for the observed death rate.
Have you seen the theory that the reason so many young fit people died in 1918 is because they were given a vaccine - can’t remember the details but think it involved horses and encephalitis or meningitis. I expect you could find a video on it on bitchute or brand new tube etc?
Pretty sure you are confusing two different stories if illness and sources. First and very plausible is that animals shipped across the Atlantic Ocean along with troops in close quarters with illness and death contributed to sickness in the soldiers that spread as they traveled to Europe and back. Nice history of animal transport conditions without human health issues.
"Newport News was the principal port for exporting horses and mules from the USA and when the USA entered the war, it built there a 77-acre complex of pens and stalls to provide for their own expeditionary force, shipping nearly 50,000 animals in under a year.
https://web.archive.org/web/20220120101257/https://maritimearchaeologytrust.org/wp-content/uploads/2021/03/Horses-at-Sea.pdf
Once on board the ships, the animals were placed in their stalls and given regular checks throughout the voyage. Despite the best efforts of the men who looked after them, many horses suffered from 'shipping fever', a form of pneumonia, and from various pulmonary complaints.
After their confinement, horses usually required several weeks to recuperate on landing. It was the job of the Remount Department and the Army Veterinary Corps to get them into shape and ready for active service.
In 1915, the Blue Cross produced ‘The Drivers' and Gunners' Handbook to Management and Care of Horses and Harness’ to provide vital information for soldiers working with artillery, ambulance and supply horses. https://web.archive.org/web/20181031174023/https://www.nam.ac.uk/explore/british-army-horses-during-first-world-war
The vaccines story is better documented as far as connection to human health and important consideration. In preparation for WW1, a massive military vaccination experiment involving numerous prior developed vaccines took place in Fort Riley, Kansas- where the first “Spanish Flu” case was reported. Two great reference links for that so the Rockefeller vaccine experiments can be verified.
Original study - A R E P O R T ON A N T I M E N I N G I T I S VACCINATION AND
OBSERVATIONS ON AGGLUTININS IN T H E BLOOD OF CHRONIC MENINGOCOCCUS CARRIERS.
BY FREDERICK L. GATES, M. D. - First Lieutenant, Medical Corps, U. S. Army.
(From the Base Hospital, Fort Riley, Kansas, and The Rockefeller Institute ./or
Medical Research, New York.) (Received for publication, July 20, 1918.)
https://web.archive.org/web/20181117191618/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2126288/pdf/449.pdf
Really nice overview w great links including study above.
https://web.archive.org/web/20200531183151/http://salmartingano.com/2020/05/the-1918-spanish-flu-only-the-vaccinated-died/
I doubt they were truly fit; the 10’s were an era of widespread tininess. A lot of photos of soldiers in WWI are startling in this regard.
More to the point, Shope makes a case that memory immunity from the spring wave was protective in the autumn wave https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1951634/ , p 174 (although this has been debated both before and since). Memory immunity protection would not be observed if deaths in the autumn wave were caused by secret bacteria vaccine trials. So, make of the case for memory immunity what you will. It’s obviously a messy story with a lot of emotion and little precision.
Brian, Is "OAS" = "Original Antigenic Sin"? It would be helpful if you fully texted your acronym before you use it. "OAS" could be "Organization of American States"; obviously not in your context. Only selecting footnotes 14 & 17 and learning about "OAS", and not "OAS", was I able to make better sense of your writing. Also, it may appeal to the non-experts to read further. Thank you for writing an eye opening "T" = thesis.
Thank you, I will fix it when I have a chance. There was a lot of editing-down of the introduction as this post was initially going to be framed in terms of my larger series, on Optional Airborne Salamanders. So the specification of the acronym was dropped by mistake. It definitely refers to Orthogonal Attic Structures.
That was a real interesting article. Thanks.
A better question would be "why spend any time on the statements of scientists when they are part of the eugenicist's agenda"? Why believe anything they say at all? Their first allegiance is to their paycheck. Why even care about what they say let alone research it and make a case against it? All of science is spell magik. It diverts us from the truth. Why are possible other causes not aired or not even mentioned? Causes like electromagnetic radiation that is making people sick? You didn't mention anything about 5G and it's rollout over the last two years which has been at a heavy clip done behind our backs and in silence. The symptoms of electromagnetic radiation probably poisoned the people in 1918 with the world wide roll out of electricity. It's amazing to me that things that are staring us in the face are never mentioned. Like the deaths from the vaccines. It's like doctors now can't put two and two together all because of that confounded paycheck.
The problem with GOF research is if the 1918 flu is not bad, they will make it bad.
Two of my former colleagues published this about 10 years ago, which is also relevant to reconsideration of the threat from the Great Influenza:
"Of the unexplained characteristics of the 1918–19 influenza pandemic, the extreme mortality rate among young adults (W-shaped mortality curve) is the foremost. Lack of a coherent explanation of this and other epidemiologic and clinical manifestations of the pandemic contributes to uncertainty in preparing for future pandemics. Contemporaneous records suggest that immunopathologic responses were a critical determinant of the high mortality rate among young adults and other high-risk subgroups. Historical records and findings from laboratory animal studies suggest that persons who were exposed to influenza once before 1918 (e.g., A/H3Nx 1890 pandemic strain) were likely to have dysregulated, pathologic cellular immune responses to infections with the A/H1N1 1918 pandemic strain. The immunopathologic effects transiently increased susceptibility to ultimately lethal secondary bacterial pneumonia. The extreme mortality rate associated with the 1918–19 pandemic is unlikely to recur naturally. However, T-cell–mediated immunopathologic effects should be carefully monitored in developing and using universal influenza vaccines."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3310443/
The part about susceptibility to unfamiliar everyday bacteria due to movement is an interesting candidate for a non-repeated environmental cofactor. The whole thing still seems a tiny bit shaky as far as the high death rates in remote or tropical areas and young adult mortality not repeating in 1958 and 1968. I will add a consideration of this in the appendix, whereas without these papers I wasn't going to take the immune overreaction theory into consideration to begin with - thanks
And this 2008 paper by the same two authors:
"Deaths during the 1918–19 influenza pandemic have been attributed to a hypervirulent influenza strain. Hence, preparations for the next pandemic focus almost exclusively on vaccine prevention and antiviral treatment for infections with a novel influenza strain. However, we hypothesize that infections with the pandemic strain generally caused self-limited (rarely fatal) illnesses that enabled colonizing strains of bacteria to produce highly lethal pneumonias. This sequential- infection hypothesis is consistent with characteristics of the 1918–19 pandemic, contemporaneous expert opinion, and current knowledge regarding the pathophysiologic effects of influenza viruses and their interactions with respiratory bacteria. This hypothesis suggests opportunities for prevention and treatment during the next pandemic (e.g., with bacterial vaccines and antimicrobial drugs), particularly if a pandemic strain–specific vaccine is unavailable or inaccessible to isolated, crowded, or medically underserved populations."
https://pdfs.semanticscholar.org/2616/22ffaf1d7da81cf685b489c0c28a0ef7165e.pdf?_ga=2.227800159.335981970.1661134700-457827293.1661134700
Thank you - this is stronger support for the secondary bacteria infection etiology than I was aware existed, especially the sources for Figure 1. That helps since as my footnote mentions I was a bit hesitant to buy into the evidence for that one.