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author

I have forwarded to JJ.

I also want to emphasize that JJ is not a “No virus person”

He has also pointed out/asked why there are only 111 full length reads in the nanopore data KIm et al.

That is likely due to the fact that nanopores selectively load smaller fragments.

For people to get these glorious long reads on nanopores, you have perform all types of size selections to get rid of the small shrapnel otherwise they consume all the pore space.

I should have better explained that oddity in KIm et al.

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I still think Couey's instincts regarding the meta are valuable - because, well, lots of people have already been making those same points, myself included: "lab leak" plays more like a deliberately staged counter-narrative, made to appear like a forbidden secret that would finally be "vindicated" in the mainstream so we could all go back to bed.

And the case for DEFUSE->WIV->SARS-CoV-2 is weak. WIV was focusing on southwest china derived genes, not northwest Laos (BANAL). And their style was way messier than the proposed SARS-CoV-2 BsmBI / BsaI map. So they aren't where it came from. Evidence continues to point to October 2019 as emergence (https://www.biorxiv.org/content/10.1101/2022.12.04.519037v1

), Wuhan was not NOT having the military games at the time.

I'm ambivalent about the case for SARS-CoV-2 really having "global transmission competence." Yes, you have FCS fidelity in all the clades, but said clades keep dying out, requiring these miraculous "resets" from B.1.1 backbones every year. Hmm. At best you could say BA.2 and 5 have finally demonstrated staying power.

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What? Nepetalactone is written by McKernan? Is that true? I'm curious because whoever wrote this blog entry didn't understand Couey's theory at all. I urge anyone interested to watch a few episodes of GigaohmBiological.com.

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Dec 9, 2022Liked by Anandamide

With all sincerity….. thank you.

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Dec 9, 2022Liked by Anandamide

Hopefully, you have forwarded this critique to him. It's the right thing to do.

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author

One other detail. While the RNA sequencing methods will miss DNA based viruses, those viruses will eventually make RNA and a surrogate of it should be captured with the above methods. Even the circular viroids have linear RCA products in the cell that would be captured and they aren’t known to infect mammals.

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Dec 10, 2022·edited Dec 11, 2022

"𝙠𝙣𝙤𝙬𝙣 𝙜𝙚𝙣𝙚𝙩𝙞𝙘 𝙥𝙧𝙚𝙙𝙞𝙨𝙥𝙤𝙨𝙞𝙩𝙞𝙤𝙣𝙨" Remember how the first waves seemed to be affecting specific groups, like Iranian parliament members?

COVID-19 – A Biological Weapon Targeting Ethnicity and Body Systems, by Larry Romanoff https://www.bluemoonofshanghai.com/politics/6371/

"𝘐𝘯 𝘵𝘩𝘦 𝘧𝘪𝘳𝘴𝘵 𝘸𝘢𝘷𝘦, [South African] 𝘋𝘳. 𝘊𝘩𝘦𝘵𝘵𝘺 𝘩𝘢𝘥 𝘰𝘯𝘭𝘺 𝘣𝘭𝘢𝘤𝘬 𝘱𝘦𝘰𝘱𝘭𝘦 𝘢𝘴 𝘱𝘢𝘵𝘪𝘦𝘯𝘵𝘴. 𝘐𝘯 𝘵𝘩𝘦 𝘴𝘦𝘤𝘰𝘯𝘥 𝘸𝘢𝘷𝘦 𝘪𝘵 𝘸𝘢𝘴 𝘮𝘰𝘴𝘵𝘭𝘺 𝘱𝘢𝘵𝘪𝘦𝘯𝘵𝘴 𝘰𝘧 𝘐𝘯𝘥𝘪𝘢𝘯 𝘥𝘦𝘴𝘤𝘦𝘯𝘵 𝘸𝘩𝘰 𝘤𝘢𝘮𝘦 𝘵𝘰 𝘩𝘪𝘮. 𝘏𝘦 𝘴𝘢𝘪𝘥, “𝘕𝘰 𝘣𝘭𝘢𝘤𝘬 𝘱𝘢𝘵𝘪𝘦𝘯𝘵𝘴 𝘢𝘯𝘺 𝘮𝘰𝘳𝘦, 𝘢𝘭𝘭 𝘐𝘯𝘥𝘪𝘢𝘯𝘴”. 𝘐𝘵 𝘸𝘢𝘴 𝘵𝘩𝘦 𝘴𝘦𝘤𝘰𝘯𝘥 𝘸𝘢𝘷𝘦 𝘵𝘩𝘢𝘵 𝘴𝘦𝘷𝘦𝘳𝘦𝘭𝘺 𝘳𝘢𝘷𝘢𝘨𝘦𝘥 𝘐𝘯𝘥𝘪𝘢, 𝘢𝘯𝘥 𝘪𝘯 𝘋𝘳. 𝘊𝘩𝘦𝘵𝘵𝘺’𝘴 𝘴𝘦𝘤𝘰𝘯𝘥 𝘸𝘢𝘷𝘦 𝘩𝘦 𝘩𝘢𝘥 𝘮𝘰𝘴𝘵𝘭𝘺 𝘐𝘯𝘥𝘪𝘢𝘯 𝘱𝘢𝘵𝘪𝘦𝘯𝘵𝘴, 𝘱𝘳𝘦𝘴𝘶𝘮𝘢𝘣𝘭𝘺 𝘵𝘩𝘦 𝘴𝘢𝘮𝘦 𝘴𝘵𝘳𝘢𝘪𝘯. 𝘐𝘯 𝘵𝘩𝘦 𝘵𝘩𝘪𝘳𝘥 𝘸𝘢𝘷𝘦, 𝘵𝘩𝘦𝘳𝘦 𝘸𝘦𝘳𝘦 𝘢𝘭𝘮𝘰𝘴𝘵 𝘯𝘰 𝘣𝘭𝘢𝘤𝘬 𝘰𝘳 𝘐𝘯𝘥𝘪𝘢𝘯 𝘱𝘢𝘵𝘪𝘦𝘯𝘵𝘴; 𝘪𝘯𝘴𝘵𝘦𝘢𝘥, 𝘵𝘩𝘦𝘺 𝘸𝘦𝘳𝘦 “𝘢𝘭𝘭 𝘸𝘩𝘪𝘵𝘦 𝘢𝘯𝘥 𝘔𝘶𝘴𝘭𝘪𝘮”. 𝘠𝘰𝘶 𝘤𝘢𝘯 𝘳𝘦𝘤𝘢𝘭𝘭 𝘵𝘩𝘢𝘵 𝘪𝘯 𝘵𝘩𝘦 𝘜𝘚, 𝘵𝘩𝘦 𝘧𝘪𝘳𝘴𝘵 𝘸𝘢𝘷𝘦 𝘦𝘴𝘱𝘦𝘤𝘪𝘢𝘭𝘭𝘺 𝘢𝘧𝘧𝘦𝘤𝘵𝘦𝘥 𝘣𝘭𝘢𝘤𝘬𝘴. 𝘞𝘪𝘵𝘩 𝘊𝘩𝘪𝘯𝘢, 𝘊𝘖𝘝𝘐𝘋 𝘸𝘢𝘴 𝘪𝘯𝘪𝘵𝘪𝘢𝘭𝘭𝘺 100% 𝘊𝘩𝘪𝘯𝘦𝘴𝘦-𝘴𝘱𝘦𝘤𝘪𝘧𝘪𝘤 𝘶𝘯𝘵𝘪𝘭 𝘵𝘩𝘦 𝘷𝘪𝘳𝘶𝘴 𝘮𝘶𝘵𝘢𝘵𝘦𝘥. 𝘛𝘩𝘪𝘴 𝘵𝘰𝘹𝘪𝘤𝘪𝘵𝘺 𝘰𝘧 𝘵𝘩𝘦 𝘴𝘱𝘪𝘬𝘦 𝘱𝘳𝘰𝘵𝘦𝘪𝘯 𝘵𝘰 𝘢 𝘱𝘢𝘳𝘵𝘪𝘤𝘶𝘭𝘢𝘳 𝘣𝘰𝘥𝘺 𝘴𝘺𝘴𝘵𝘦𝘮 𝘮𝘢𝘺 𝘣𝘦 𝘶𝘯𝘪𝘷𝘦𝘳𝘴𝘢𝘭. 𝘚𝘰𝘮𝘦 𝘤𝘰𝘶𝘯𝘵𝘳𝘪𝘦𝘴 𝘸𝘦𝘳𝘦 𝘦𝘹𝘱𝘰𝘴𝘦𝘥 𝘵𝘰 𝘮𝘰𝘳𝘦 𝘴𝘵𝘳𝘢𝘪𝘯𝘴 𝘵𝘩𝘢𝘯 𝘰𝘵𝘩𝘦𝘳𝘴, 𝘯𝘰𝘵 𝘢𝘭𝘭 𝘸𝘪𝘵𝘩 𝘵𝘩𝘦 𝘴𝘢𝘮𝘦 𝘯𝘶𝘮𝘣𝘦𝘳 𝘰𝘧 𝘴𝘵𝘳𝘢𝘪𝘯𝘴 (𝘸𝘢𝘷𝘦𝘴), 𝘢𝘯𝘥 𝘪𝘯 𝘰𝘵𝘩𝘦𝘳 𝘤𝘰𝘶𝘯𝘵𝘳𝘪𝘦𝘴 𝘰𝘵𝘩𝘦𝘳 𝘮𝘢𝘫𝘰𝘳 𝘣𝘰𝘥𝘺 𝘴𝘺𝘴𝘵𝘦𝘮𝘴 𝘸𝘦𝘳𝘦 𝘢𝘧𝘧𝘦𝘤𝘵𝘦𝘥, 𝘵𝘩𝘦 𝘳𝘦𝘱𝘳𝘰𝘥𝘶𝘤𝘵𝘪𝘷𝘦 𝘴𝘺𝘴𝘵𝘦𝘮 𝘣𝘦𝘪𝘯𝘨 𝘰𝘯𝘦. 𝘈𝘭𝘴𝘰, 𝘵𝘩𝘦 𝘦𝘵𝘩𝘯𝘪𝘤-𝘴𝘱𝘦𝘤𝘪𝘧𝘪𝘤𝘪𝘵𝘺 𝘰𝘧 𝘥𝘪𝘧𝘧𝘦𝘳𝘦𝘯𝘵 𝘸𝘢𝘷𝘦𝘴 𝘪𝘯 𝘥𝘪𝘧𝘧𝘦𝘳𝘦𝘯𝘵 𝘤𝘰𝘶𝘯𝘵𝘳𝘪𝘦𝘴 𝘮𝘢𝘺 𝘣𝘦 𝘶𝘯𝘪𝘷𝘦𝘳𝘴𝘢𝘭 𝘣𝘶𝘵 𝘸𝘦 𝘥𝘰𝘯’𝘵 𝘩𝘢𝘷𝘦 𝘵𝘩𝘦 𝘪𝘯𝘧𝘰𝘳𝘮𝘢𝘵𝘪𝘰𝘯 𝘣𝘦𝘤𝘢𝘶𝘴𝘦 𝘵𝘩𝘦 𝘮𝘦𝘥𝘪𝘢 𝘤𝘰𝘯𝘵𝘳𝘰𝘭 𝘵𝘩𝘦 𝘯𝘢𝘳𝘳𝘢𝘵𝘪𝘷𝘦 𝘢𝘯𝘥 𝘵𝘩𝘦𝘴𝘦 𝘵𝘰𝘱𝘪𝘤𝘴 𝘢𝘳𝘦 𝘴𝘶𝘣𝘫𝘦𝘤𝘵 𝘵𝘰 𝘢 𝘧𝘶𝘭𝘭 𝘯𝘦𝘸𝘴 𝘦𝘮𝘣𝘢𝘳𝘨𝘰."

Briefing by Lieutenant General Igor Kirillov, Head of Nuclear,Biological and Chemical Protection Troops of the Russian Armed Forces https://telegra.ph/Briefing-by-Lieutenant-General-Igor-Kirillov-Head-of-NuclearBiological-and-Chemical-Protection-Troops-of-the-Russian-Armed-Force-08-04

"𝘈𝘤𝘤𝘰𝘳𝘥𝘪𝘯𝘨 𝘵𝘰 𝘰𝘶𝘳 𝘦𝘹𝘱𝘦𝘳𝘵𝘴, 𝘵𝘩𝘪𝘴 𝘪𝘴 𝘦𝘷𝘪𝘥𝘦𝘯𝘤𝘦𝘥 𝘣𝘺 𝘵𝘩𝘦 𝘶𝘯𝘤𝘩𝘢𝘳𝘢𝘤𝘵𝘦𝘳𝘪𝘴𝘵𝘪𝘤 𝘷𝘢𝘳𝘪𝘢𝘣𝘪𝘭𝘪𝘵𝘺 𝘰𝘧 𝘵𝘩𝘦 𝘨𝘦𝘯𝘰𝘷𝘢𝘳𝘪𝘢𝘯𝘵𝘴 𝘵𝘩𝘢𝘵 𝘤𝘢𝘶𝘴𝘦 𝘥𝘪𝘧𝘧𝘦𝘳𝘦𝘯𝘵 𝘱𝘦𝘢𝘬𝘴 𝘪𝘯 𝘵𝘩𝘦 𝘪𝘯𝘤𝘪𝘥𝘦𝘯𝘤𝘦 𝘰𝘧 𝘤𝘰𝘳𝘰𝘯𝘢𝘷𝘪𝘳𝘶𝘴𝘦𝘴, 𝘴𝘪𝘨𝘯𝘪𝘧𝘪𝘤𝘢𝘯𝘵 𝘥𝘪𝘧𝘧𝘦𝘳𝘦𝘯𝘤𝘦𝘴 𝘪𝘯 𝘭𝘦𝘵𝘩𝘢𝘭𝘪𝘵𝘺 𝘢𝘯𝘥 𝘤𝘰𝘯𝘵𝘢𝘨𝘪𝘰𝘶𝘴𝘯𝘦𝘴𝘴, 𝘶𝘯𝘦𝘷𝘦𝘯 𝘨𝘦𝘰𝘨𝘳𝘢𝘱𝘩𝘪𝘤𝘢𝘭 𝘥𝘪𝘴𝘵𝘳𝘪𝘣𝘶𝘵𝘪𝘰𝘯, 𝘢𝘯𝘥 𝘵𝘩𝘦 𝘶𝘯𝘱𝘳𝘦𝘥𝘪𝘤𝘵𝘢𝘣𝘭𝘦 𝘯𝘢𝘵𝘶𝘳𝘦 𝘰𝘧 𝘵𝘩𝘦 𝘦𝘱𝘪𝘥𝘦𝘮𝘪𝘤 𝘱𝘳𝘰𝘤𝘦𝘴𝘴 𝘢𝘴 𝘢 𝘸𝘩𝘰𝘭𝘦. 𝘐𝘵 𝘢𝘱𝘱𝘦𝘢𝘳𝘴 𝘵𝘩𝘢𝘵 𝘥𝘦𝘴𝘱𝘪𝘵𝘦 𝘦𝘧𝘧𝘰𝘳𝘵𝘴 𝘵𝘰 𝘤𝘰𝘯𝘵𝘢𝘪𝘯 𝘢𝘯𝘥 𝘪𝘴𝘰𝘭𝘢𝘵𝘦 𝘵𝘩𝘦 𝘥𝘪𝘴𝘦𝘢𝘴𝘦, 𝘵𝘩𝘦 𝘱𝘢𝘯𝘥𝘦𝘮𝘪𝘤 𝘪𝘴 𝘣𝘦𝘪𝘯𝘨 𝘢𝘳𝘵𝘪𝘧𝘪𝘤𝘪𝘢𝘭𝘭𝘺 𝘧𝘶𝘦𝘭𝘭𝘦𝘥 𝘣𝘺 𝘵𝘩𝘦 𝘪𝘯𝘵𝘳𝘰𝘥𝘶𝘤𝘵𝘪𝘰𝘯 𝘰𝘧 𝘯𝘦𝘸 𝘷𝘢𝘳𝘪𝘢𝘯𝘵𝘴 𝘰𝘧 𝘵𝘩𝘦 𝘷𝘪𝘳𝘶𝘴 𝘪𝘯 𝘢 𝘱𝘢𝘳𝘵𝘪𝘤𝘶𝘭𝘢𝘳 𝘳𝘦𝘨𝘪𝘰𝘯."

ACE2 coding variants in different populations and their potential impact on SARS-CoV-2 binding affinity DOI: 10.1016/j.bbrep.2020.100798

New insights into genetic susceptibility of COVID-19- an ACE2 and TMPRSS2 polymorphism analysis DOI: 10.1186/s12916-020-01673-z

"Putin Questions US Air Force DNA Collection From Ethnic Russians" https://archive.vn/tsnMy#selection-411.6-411.70

The CDC admitted over 75% of cases had 4+ co-morbidities. Take away the co-morbidities and "/with" cases and you're left with a normal flu season. The initial deaths in the West were driven by midazolam and criminal neglect. For the bulk of the population, CoV is just a numbers game based on a meaningless test. It's easy to understand where the "virus deniers" are coming from. When we look at the whole picture, at best, we're dealing with perhaps a whole suite of bioweapons being deployed in specific areas, at specific times, targeting specific groups, the one with the largest distribution being almost totally benign. The same seems like it may be true of the "vaccine."

All the lab leak hypothesis does is let the perps off the hook in favor of an "Act of God".

Dilyana Gaytandzhieva has been documenting US biolab and warfare activity in Tblisi for some time. The civilian employees have diplomatic privileges, including the "diplomatic bag". https://dilyana.bg See: The Luger Center leaks

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Appreciate this sober and respectful piece. It’s the way dialogue ought to happen. Kudos to you on sharing your expertise in this way!

What do you make of the plausibility of the hypothesis that there may have been multiple CV ICs released in different locations, at different times—all having largely similar sequences, but with smaller variation, bearing FCS, and having enough homologous to trigger PCR primers? This could account for reach of the FCS signature.

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Thank you for this article. Although I don’t understand all the jargon, I get what you’re saying. I had a feeling JJ wasn’t fully correct when I first heard him theorise but I didn’t have the knowledge to refute.

I agree this virus is unlike anything else - my family had it in Nov/Dec’19 (U.K.) and it frightened the life out of me as the symptoms were weird, out of order and unlike anything I’d ever had described to me by a patient ( I’m a retired GP). I remember saying to my husband that we should tell people that we’d had the flu as we wouldn’t get enough sympathy for what we’d been through, even though I knew it wasn’t the flu!

Can you explain how omicron came to be - as far as I understand it’s sequence doesn’t fit with any form of evolution and BA1 & BA2 between them conveniently covered all the escape mutations? Thanks.

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I thought this article at least indicated that 1/3 of covid deaths were really due to pneumococcal bacteria. The other 2/3 could maybe be explained by something else.

https://academic.oup.com/jid/article/225/10/1710/6164926

When the FDA was so slow to approve PCR tests in early 2020, that seemed to be due to fundamental scientific issues.

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A lot beyond my ken but I got the defense of sequencing when findings are so widespread and consistent. Also, you point out that creating a virus that can be treated with a pre-existing customized technology can a profit opportunity with the right regulatory capture (that in my judgment is what happened with SARS2; and I wish you and David Martin could converge on this).

Lab origin is certainly plausible. I do kind of wonder if JJ got a visit off-hours ....

I would very much like to have you address the intrinsic safety of mRNA vaccines. I'm still trying to find a reference for "the animals all died" in trials. I will never take an mRNA injection until ten years of testing has been done. We all know what VAERS says, but what are dangers that were known and swept aside?

Finally, with an N=1, I'm unvaxxed and had Covid in February, and it was unlike any virus I ever had before; I had shortness of breath, myocarditis, and ached all over. I recovered fairly quickly, but was left with the impression that there was something synthetic, like a buzz saw, about this virus. Others have felt the same way. The super-antigenic spike with enhanced ACE-2 binding capability?

We also have to find out what is in the shots. I believe the doctors who are finding graphene oxide and a strange assortment of minerals in them. The contracts do not permit examination, but it must be done.

Cheers.

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Hi Kevin,

I've been reading this again and I would like to share a few perspectives. You said "the swarming effect wont dilute this out fast enough to prevent global transmission". This would imply, it seems to me, that according to your thesis, until a given "novel/leaked" strain dilutes itself into the background of endemic viruses, correct me if I am wrong, it would transmit and proliferate itself globally maintaining its genomic traits (in this case, its virulence). In other words, as you said "the rate of divergence in the swarm is too slow to fizzle out global spread of pathogenic variants".

You also said the following:

"The sequencing data clearly shows the duration of each variants and how long this clade remained the dominant member of the swarm. I see no reason a more virulent leaked clone couldn’t last just as long and lap the globe.

There is now a $100B incentive for a Biotech company or state actor to create a new virus and profit from the vaccines or testing industries that will quickly reboot for the next leak."

These statements would imply that any such genetic sequences, created in a lab via artificial means, would proliferate and propagate themselves and behave as if they were already dominant stable structures of the ecosystem, which is completely not true. The problem that I see is that you are conflating the general dynamics of such systems when they are already in equilibrium, as you said, "The sequencing data clearly shows the duration of each variants and how long this clade remained the dominant member of the swarm", and applying that knowledge to whatever new lab made variation comes around, as if they could, whenever they want to, find such a dominant structure via cell culture, animal passage, computer simulations and the use of molecular biology tools. In fact, I would argue, it is impossible to do so. We cannot know via any of those means, if the genome that we are studying has the potential to become dominant in any way, once it is in nature.

Problems that I see with this and farther explanation of my perspective:

1) The concept of transmission chain and the conclusions we derive from it are not accurate. We always start to acquire genetic sequencing data when the general dynamics of the system are already in place and most likely the genetic materials that we are trying to measure/track are already ubiquitous.

Waves in this case can very easily be seen as modulatory effects of such dynamical system, or in other words, quasi-stable states of proliferation guided by seasonality and related cycles driven by a myriad of other environmental factors that cannot be properly isolated from one another and are completely heterogeneous. Thus, what is "traveling" are not waves of infection/virions, but rather, waves of information that may produce proliferation of virions with given genomic traits under very particular conditions.

2) There is something extremely important at this stage of our understanding of this phenomena in relation to your point, "Much of the sequencing surveillance is simply mapping to a reference genome and likely only seeing dominant members of the swarm with over 5% allele frequency".

This extremely important point is the fact that the most dominant genomes are not necessarily the most relevant ones for the coherence and behavior of the whole dynamics of the system, as it moves from equilibrium, to quasi-equilibrium, to proliferation phases. This point is quite complex and there is not much in relation to it within the literature, if any, so I will leave it here. However this could very well open a whole new line of research in my opinion. Although we would need to re-evaluate and better characterize the foundational theories and language used to describe viral dynamics for this line of research to occur, which is not very likely because we are extremely bias and quite dogmatic in the field of virology, due to its links with epidemiology, public health and the whole industry.

3) Coming back to point (1), in order to have [waves of information that may produce proliferation of virions] within the ecosystem (in this case the human ecosystem), such virions must be stable, that is, the genomic traits expressed by such signals must conform to all other interactions in the network. This would include modulatory phase transitions within the network of related dominant and subdominant strains (that as I said in point (2), we may not even be able to measure), as well as regulatory processes related to the microbiota and their inherent dynamics, in conjunction with the extremely complex and heterogeneous network of interactions that belongs to the immune system and its network of communications and information transfer in different cohorts of the population, as well as in different species and related signaling pathways that travel throughout the ecosystem in a myriad of different ways. That is, an extremely complex system, which cannot be predicted with our current understanding, and perhaps it never will be.

This whole set of dynamic equilibria would create the potential landscape for the evolutionary dynamics of all genetic variations that are allowed to proliferate, modulate and travel throughout the system, which in this case would be the whole globe, if we are making reference to coronavirus sequences from which we can generate tangible and measurable isolates. That is to say, we cannot predict if a given genome would be able to travel in this network. For sure we cannot make it to be a dominant and permanent feature of the network. Imagining that we can, is, quite frankly, a bit delusional if we think about it more carefully.

THEREFORE, if a lab leak or some other contamination event happens, there will never be a spread of such genomic traits until they have adapted themselves to the general dynamics of the system, which may take years, decades, or even never happen. And that is why I would call it a contamination event, not a lab leak. In the case of a biological agent that is capable of limited spread with some degree of virulence, what moves are waves of non-equilibrium states, and therefore a biological agent would not be able to proliferate as a disease-causing agent beyond the second to third layer of direct exposure to the agent. This of course is an estimate, it will be different for different potential agents, if they are indeed possible in any way other than an extremely high dose directly applied to the given target, like we do in animal experiments. The limited spread will occur due to the lost of the given characteristics that promote such non-equilibrium state (e.g. purity, quantity, concentration, proteomic transient alterations, transient genomic patterns...).

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for me , on the ground, this infection often appeared novel. Yes in hindsight, and yes through a distorted lens of hype. But the process of crumping at day 8 after symptoms I have never witnessed before. And i atched it quite a few times. VEry repeatable. I knew I needed to be watching people closely around day 8.

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No matter how much you post this on X, Couey, Nick and most of PANDA won't care. I posted it and broke it down for them multiple times on SLACK. They won't read it, and they won't understand your point. They aren't there to learn, they are there to be "right" to people who can't tell the difference. Also pretty sure they memory holed your sequencing presentation, unless I missed them publishing it.

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My housemate had fever, aches & pains, and a week long illness.

I looked after them, feeding them etc, and caught it 5 days into their illness.

I had swollen to tf tonsils and snot / spit going for 3-4 days but nothing else. Same week long unwellness, and it all started with a bowl of soup tasting weird af.

My housemate vaxed x2 + boosted, me unvaxed.

Sounds like you had a lot worse.

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Lab origin or lab leak?

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