As the other co-author, (of the peer reviewed work, not this article or the others on this substack, which are all Dan's work. And, in fact, he really did most of the work on that peer reviewed article, too, I just acted like an encouraging major professor with a student who picked his own project and whose work and energy did the work, with minor supervision.) I am hoping to engage with the readers. Dan was ahead of me, in spite of, and maybe because of my formal training as a microbiologist, as I worked with bacteriophage T4, not prone to being a quasi species. Or, staring in the 1970s. Loved this above piece, but perhaps I can add something by being available as a sort of "ask the professor" thread. After all, I did teach Molecular Virology at the University level, before designing and implementing internationally used genetic databases.
I will NEVER criticize or even critique answers. All I ask is for those to whom the material I present is well known, and there will be some, that I not be criticized for that.
So, when I say I did not see swarms, in my graduate work, it was because we wanted pure genomes which we could get by diluting phage solutions and spreading them on a lawn of bacterial hosts, in which one phage would eat a hole, leaving gobs of copies of itself.
This was the DNA phage T4 which recombines a lot, but whose genome is normally pretty stable.
The questions are:
1. What is different from T4 in flu and coronavirus?
2. Would a plaque (or equivalent) represent one genome, for these other viruses, of not, why not?
3. What experiments, or procedures should be done to measure swarms in RNA viruses?
This is the level of understanding the world needs of this virus, and which has been lacking to date. The entire field of microbiology has lacked a theorist who can make the scales fall from their eyes. and this is the price we pay.
Is it your theory that people in Wuhan were given these LAVs as part of a human experiment and somehow they were infected by the man made virus and it spread so quickly because it reverted to the original highly pathogenic virus?
I'm new to all this language but fascinated beyond my imagination at what is going on. Can you first please tell me what exactly the furin cleavage site is and what is does ? This paper says that it occurs naturally in coronaviruses but I thought it was not a natural occurrence instead it is n insertion.
Mr. Sirotkin...This is simply incredible work. I'm going to have to read this about 12 more times for it to absorb into the limited bandwidth I have between the ears. A few questions, but let me know if I'm being a pest. Incredibly presciently, you published this article and discussed the issue of the Vero cells vs. the Calu-3 LONG BEFORE this seems to have become a defining issue of BA.2.86; it shuns Vero cells, but loves Calu-3 cells. And I imagine that is not good. Nice crystal ball you have there.
Were the folks at Wuhan actively trying to produce an FCS from the starting point of a bat virus?
Is the final deattenuated virus a bat virus that is adapted for human transmission?
Amazing hubris to be playing with this stuff. Thanks for the education. I'm just blown away by all this.
Wow...this is deep. I'm a bit of a dolt, but can you clarify something for me?
This phrase caught my attention "...long way from surgically splicing precise nucleotides in-and-out, which led to the cryptic emergence of the FCS in small minority subpopulations"
Are you saying that the FCS was not specifically inserted in the Wuhan lab, but had originated earlier in what amounted to 'gain of function' experiments in other labs as the swarm mutated haphazardly encouraged by human manipulation? Thanks for any clarification you can provide.
“Each and everyone one of these arrogant old hacks was drawn into the siren song of multi-billion dollar defense and pharmaceutical contracts long ago, and they’re going to remain pushing for a fascist and entirely ineffective vaccination program because they’re rotten, filthy, diseased whores, and that is exactly what they are being paid to do.”
Just dropping by a year later to say “thanks”. Vital and prescient read, and perhaps even more relevant today than it was a year ago. Thanks again.
I've been re-reading this and the Golden Silkworms articles. Is my understanding of this correct?
* viral mutation rates are greatly increased because of the quasispecies nature of an infection. Whenever virons with two different RNA sequences infect the same cell, they can recombine per https://www.nature.com/articles/nrmicro2614
* could an mRNA vaccine combined with an active infection allow cross-combining vaccine-mRNA spike sequences with active viral sequences? Since the vaccine uses psuedo-uridine, which has lower copy accuracy, this would increase mutation rates in the spike protein
* using drugs such as molnupiravir that increase viral mutation rates are ill-advised
As the other co-author, (of the peer reviewed work, not this article or the others on this substack, which are all Dan's work. And, in fact, he really did most of the work on that peer reviewed article, too, I just acted like an encouraging major professor with a student who picked his own project and whose work and energy did the work, with minor supervision.) I am hoping to engage with the readers. Dan was ahead of me, in spite of, and maybe because of my formal training as a microbiologist, as I worked with bacteriophage T4, not prone to being a quasi species. Or, staring in the 1970s. Loved this above piece, but perhaps I can add something by being available as a sort of "ask the professor" thread. After all, I did teach Molecular Virology at the University level, before designing and implementing internationally used genetic databases.
I will NEVER criticize or even critique answers. All I ask is for those to whom the material I present is well known, and there will be some, that I not be criticized for that.
So, when I say I did not see swarms, in my graduate work, it was because we wanted pure genomes which we could get by diluting phage solutions and spreading them on a lawn of bacterial hosts, in which one phage would eat a hole, leaving gobs of copies of itself.
This was the DNA phage T4 which recombines a lot, but whose genome is normally pretty stable.
The questions are:
1. What is different from T4 in flu and coronavirus?
2. Would a plaque (or equivalent) represent one genome, for these other viruses, of not, why not?
3. What experiments, or procedures should be done to measure swarms in RNA viruses?
(Happy to discuss all this.)
Hints:
https://en.wikipedia.org/wiki/Whole_genome_sequencing
https://en.wikipedia.org/wiki/Polymerase_chain_reaction
For those more familiar with these technology, what role would primer choice make?
This is the level of understanding the world needs of this virus, and which has been lacking to date. The entire field of microbiology has lacked a theorist who can make the scales fall from their eyes. and this is the price we pay.
Yikes, could they (CDC,NIH,NIAID,Gates, Fauci, Daszak, etc) all be in on it just for the money? I can't wrap my head around that...
Is it your theory that people in Wuhan were given these LAVs as part of a human experiment and somehow they were infected by the man made virus and it spread so quickly because it reverted to the original highly pathogenic virus?
Awesome, thanks!!
I'm new to all this language but fascinated beyond my imagination at what is going on. Can you first please tell me what exactly the furin cleavage site is and what is does ? This paper says that it occurs naturally in coronaviruses but I thought it was not a natural occurrence instead it is n insertion.
Mr. Sirotkin...This is simply incredible work. I'm going to have to read this about 12 more times for it to absorb into the limited bandwidth I have between the ears. A few questions, but let me know if I'm being a pest. Incredibly presciently, you published this article and discussed the issue of the Vero cells vs. the Calu-3 LONG BEFORE this seems to have become a defining issue of BA.2.86; it shuns Vero cells, but loves Calu-3 cells. And I imagine that is not good. Nice crystal ball you have there.
Were the folks at Wuhan actively trying to produce an FCS from the starting point of a bat virus?
Is the final deattenuated virus a bat virus that is adapted for human transmission?
Amazing hubris to be playing with this stuff. Thanks for the education. I'm just blown away by all this.
Wow...this is deep. I'm a bit of a dolt, but can you clarify something for me?
This phrase caught my attention "...long way from surgically splicing precise nucleotides in-and-out, which led to the cryptic emergence of the FCS in small minority subpopulations"
Are you saying that the FCS was not specifically inserted in the Wuhan lab, but had originated earlier in what amounted to 'gain of function' experiments in other labs as the swarm mutated haphazardly encouraged by human manipulation? Thanks for any clarification you can provide.
“Each and everyone one of these arrogant old hacks was drawn into the siren song of multi-billion dollar defense and pharmaceutical contracts long ago, and they’re going to remain pushing for a fascist and entirely ineffective vaccination program because they’re rotten, filthy, diseased whores, and that is exactly what they are being paid to do.”
Just dropping by a year later to say “thanks”. Vital and prescient read, and perhaps even more relevant today than it was a year ago. Thanks again.
These researchers say it looks like SARS-Cov-2 jumped to mice, then back to people. Seems compelling to me, but I'm not an expert.
December 14th, 2021
Evidence for a mouse origin of the SARS-CoV-2 Omicron variant
https://www.biorxiv.org/content/10.1101/2021.12.14.472632v1.full.pdf
I've been re-reading this and the Golden Silkworms articles. Is my understanding of this correct?
* viral mutation rates are greatly increased because of the quasispecies nature of an infection. Whenever virons with two different RNA sequences infect the same cell, they can recombine per https://www.nature.com/articles/nrmicro2614
* could an mRNA vaccine combined with an active infection allow cross-combining vaccine-mRNA spike sequences with active viral sequences? Since the vaccine uses psuedo-uridine, which has lower copy accuracy, this would increase mutation rates in the spike protein
* using drugs such as molnupiravir that increase viral mutation rates are ill-advised
I can't explain to you why some thing that isn't vaguely scientific and has no basis in science, isn't scientific man.
he is hand waving and making shit up, there is a reason there's nothing published peer reviewed and he is trying to invent something out of his ass.
If you can't see that I am sorry I can't help you
It seems like this aligns pretty well with the Ethical Skeptic's work: https://theethicalskeptic.com/2021/11/15/chinas-ccp-concealed-sars-cov-2-presence-in-china-as-far-back-as-march-2018/
Does that make sense?