These are my thoughts on the debate as to whether viruses exist or not, taking as ‘inspiration’ the video debate between Steve Kirsch and Andrew Kaufman [here] and Steve’s Substack article: here.
I have no qualifications in biology and am certainly no expert in isolation or gene sequencing techniques but these are not the only perspectives.
Priorities:
- The laws of Physics must be obeyed
- Statistical principles must given due prominence
- Theoretical frameworks must be self-consistent
- Arguments must be logically sound
- Language should not be ambiguous or misleading
- Epidemiology needs an explanation
- Attempts should be made to quantify observations and statements
- Philosophical musings concerning the nature of existence are irrelevant
- Arguments should not be rejected for failing to adhere to The Scientific Method.
“Over 130 years of data; none of it inconsistent with virology“
What?! Almost nothing that happens is consistent with virology. The industry just adapts the ideology to fit the data
- Not everybody gets ill so the idea of immunity was conceived with no proof
- Genomes are inconsistent thereby giving rise to the (fuzzy) concept of a variant
- People don’t get sick immediately after contact so an incubation period is assumed but never proven
- People get ill without contact with other sick people so .. asymptomatic transmission!
- Flu disappears in winter. Latency is proposed but not proven.
- Novel behaviours or symptoms are not deemed inconsistent but immediately assigned to a new variant without justification
The biggest inconsistencies are with the epidemiology:
- Clinical trials consistently fail, eg Rosenau – this needs an explanation
- Doctors, for example, see ten times as many sick people as the rest of us but don’t get ill ten times as often
- Sickness within families does not seem to increase the likelihood of becoming ill
- In situations where the population density is high we would expect an increase likelihood of becoming ill but it is in fact slightly reduced
- Disease is seasonal and correlated with latitude and changes in the weather – Why?
- ‘Transmission’ of influenza has historically happened faster than the common mode of transport and has not followed the usual travel infrastructure
- Conjoined twins do not catch flu off each other
- Lockdowns don’t work
None of these points require any expertise at all in virology to understand or even the idea of a small particle. They are all inconsistent the idea of transmission per se regardless of any assumptions concerning the mechanism.
A common argument is that doctors somehow acquire immunity by constant contact with sick people and without getting ill. This brings their infection rate down to the precise value it was if they didn’t have the immunity but avoided contact with patients. There is no evidence for this apart from the actual data which we are trying to explain in the first place.
This is clear bunk but circular arguments such as this seems to be sufficient for those who are already invested in the idea of viruses and so the contagion myth continues.
“No virus has ever been isolated!”
“We never say that fire and gravity cannot exist because you cannot ‘isolate’ them.” Kirsch
We hear this a lot from those in the medical profession with gravity, photons and electrons being common examples. This therefore needs addressing.
Gravity is known by its effect on real physical objects and the concept of gravity is verified by quantitative predictions. The speed of falling objects can be measured precisely and its future trajectory can be accurately computed. Same goes for electricity.
The idea of a ‘force’ is a theoretical concept and I am not sure what it means to say that a theoretical concept ‘exists’. Certainly its existence is not qualitatively the same as the existence of an apple, say. The word ‘existence’ needs to be qualified if the context is not clear. The conflation used above is a distraction.
A virus is supposed to be a real thing consisting of real physical material and so the idea of physical existence is pertinent. Viruses are assumed to be too small to see but being part of the physical world they should be amenable to investigation by physical means, they should leave some sort of physical ‘footprint’.
Some method of characterisation and classification is needed and the virologists seem to have decided upon the result of genome sequencing as a way of doing this. As far as I can understand, they are therefore defining a ‘virus’ as the outcome of a series of chemical reactions.
This is fine as far as it goes but these sequences must be shown to have some biological significance or else what is the point? There needs to be some credible model that relates genome sequence to biological action but it seems that none is available. ‘Association’ is not good enough as, given long enough sequence, there will always be some sort of association to be found somewhere.
Koch’s postulates
These are often suggested as being appropriate to ascertain whether or not an organism causes a disease. Postulate 3, however, reads “The cultured microorganism should cause disease when introduced into a healthy organism.”. So in order to determine if an organism causes disease we must first see if it causes a disease in addition to the other three postulates!
Clearly the postulates are not fit for purpose. This was not their original intent.
In addition to this, the Postulates clearly take the process of ‘isolation’ as a given. They were formulated to deal with bacteria which are easily visible and characterised by outward form.
Koch’s postulates are therefore not suitable for virology.
Replication of the sequence in millions of people who were diagnosed with COVID
“Each lab is given a sample from an infected person and asked to identify any novel pathogen that has not been seen before using only the data in the sample. In over 100 countries, the genome sequences (which are nearly 30,000 nucleotides long) came back that were virtually identical. This can’t happen by chance. AFAIK, there is only one way it can happen: the same base pathogen is infecting people all over the world” – Steve Kirsch
So on the information we have here:
- The labs were only given data from sick people
- There was therefore no control
- They were specifically told to ignore influenza ‘virus’
- The sequenced genomes were not identical
Saying that the samples were ‘virtually identical’ is surely persuasive language as opposed to scientific. What is required is some way of quantifying the similarity of two sequences.
Some sort of meaningful, well defined metric is required if we are to compare different genome sequences. To simply give a percentage match is wholly inadequate as we don’t know what the percentage means in biological terms.
A early sequencing of SARS-CoV-2 sequence gave an 89% match to some bat-sequence. Are these genomes sufficiently similar? Why?
- Is the total percentage all that matters?
- Are some pairs more important than others?
- Are all sub-sequences equally likely?
- Does the genome have random characteristics or is there necessarily some structure?
- Are there critical areas in the genome? Is there chaotic behaviour?
- Do similar sequences necessarily have similar biological function and if so how do we measure similarity of biological function?
- What are the criteria that determine whether a sequence is a variant or not?
If these issues have been addressed then they are not in common circulation.
“This can’t happen by chance. AFAIK, there is only one way it can happen: the same base pathogen is infecting people all over the world.” – Kirsch
But transmission by breath, say, has never been established and so cannot be cited as a cause. This result is being cited as both evidence and cause at the same time.
‘AFAIK’ is clearly subjective and will change with further knowledge. If we only ever explain things in terms of things we already know then we will never progress, ever.
Our knowledge of biology and even physics is far from being complete and results such as this may be indications of such. To say “I have a fixed and finite set of ideas and I am determined to explain everything in terms of these” is clearly short sighted to put it mildly.
“If viruses don’t exist, how would you explain this?” Transmission was not demonstrated and nor was the ability to cause disease and nor was the actual existence of a particle, merely similar genome sequences.
Universal agreement on the structure of SARS-CoV-2
“So if a virus doesn’t exist, how can there be such universal agreement among all researchers with no dissent whatsoever?” – SK
Agreement has been reached on the structure of something but that thing was never shown to be infectious and was never shown to cause disease and so it cannot be called a ‘virus’.
This is frustrating. The issue here is whether a small piece of RNA can actually cause a disease in a living human being but all that is happening is that geneticists are finding interesting patterns in RNA and agreeing with each other. They are, as Christine Massey would put it, just “doing stuff with cells“.
All this is tangential to the main contention. There is no point on determining the structure of something if it has nothing to do with causing a disease.
Quantitative PCR (qPCR)
“Viruses replicate” – SK
Triggering language again. No particle has been shown to cause disease and therefore no particle can be said to be a virus. This is not pedantry. The constant use of such language tends to bypass cognitive censorship and establish the notion of a virus within the mind of the listener without evidence or argument. We are thus left with an entire planet full of people who believe in viruses – but they don’t know why.
Try: “RNA replicates“. No, it doesn’t. Cells replicate and cells manufacture RNA. However, RNA itself does not and cannot replicate. Again, this might seem picky but the constant use of sloppy language reinforces sloppy (and incorrect) ideas.
The claim that RNA replicates enforces the notion of precision and omits the suggestion that there is any other influence on the sequence other than that of the original sample. This is of course not true and the technology of gene-editing is testament to that.
Again, the notion of replication is a sleight of hand, a useful ‘wallpaper’ to cover the cracks in the narrative. It gives the impression that the same thing happens in vitro as happens in vivo. If this is what virologists are claiming them we would like to see proof of this please.
Similarly, the idea of ‘mutation’ strongly suggests the existence of a stable sequence with minor variations from that sequence but if what we end up with is essentially lots of constantly changing sequences then nothing is really stable and so nothing is really a ‘variant’.
“You can lock these people in a room right after they are sick and the qPCR results will increase by 2 to 3 orders of magnitude. That means it is replicating.”
So the people are in a diseased state and for some reason are producing more and more of these particles whatever you want to call them. We have an association here between disease and gene sequence but no proof that it is the RNA that is causing the disease as opposed to the other way around. There was no proof of transmission here either.
“AFAIK, the rise and fall of the amount of genetic material can only explained by foreign (i.e., non-host) genetic material that is capable, either on its own or with the help of a host cell, of replication.”
The claim here is that RNA can replicate all by itself with no help of a host cell! So it is somehow pro-active in manufacturing or assembling sufficient molecular material and before generating enough energy all but itself to stick them together in the correct order?
Why is this only explained by foreign material? Why cannot the ‘host’ itself manufacture it? Human beings are quite capable of creating and folding precision molecules as in the case of proteins. A million people have similar, if not identical, proteins but it doesn’t mean that it was the proteins that made the sick.
Proteins and indeed RNA are not assembled according to a set of digital instructions but by the laws of physics and chemistry. Proteins likely assembled via resonance (Resonant recognition model) and then folded by the adoption of successive attractor states to achieve the final form.
According to Denis Noble and others, new DNA is only vaguely similar to its ‘template’ but becomes to resemble it more closely post-creation. It is therefore a teleological process whose final aim is determined by the cell itself. So the more cycles or whatever, the closer the gene sequence moves to some ‘least-energy’ attractor state.
Antibodies
“A virus can cause antibodies to be created and we can measure that.” – You have not established that it is a virus yet.
“If it isn’t a virus but is simply a reaction to external stress, then why are antibodies being created?”
I don’t know but the ‘word’ in the no-virus community is that antibodies are not antigen specific and that they are some sort of repair mechanism.
What exactly were they working on in the Wuhan Institute of Virology for the past decade?
They were doing stuff with cells the same as everybody else. They are good lab technicians who accurately report their results but just interpret them incorrectly.
Humanised mice are not humans and if no human was made sick by inhaling the breath of another person then no virus was created.
Barnstable County: how did all these people have the same sequence that replicated inside of them?
” Basically, over 1,000 healthy people congregated, and 469 then developed COVID.”
“Virology explains this. It spread between people who were congregating in close quarters, exactly as we’d expect a virus to spread.“
No. This is monster silliness now.
It is stated as a fact that it spread but spreading was not observed, it never is.
Nearly 50% of people got disease but this is not normal. There were rallies that were larger than this which, by the laws of probability, would have certainly contained sick or sickening people and yet nowhere near the same number of people succumbed. Why not?
What happened after the sick people went home to their families? Did 50% of their kin get sick? No, this never happens on this scale.
This is not consistent with virus theory but rather refutes it somewhat.
Attacks of influenza are overwhelmingly related to changes in the weather and are restricted in time and space – Influenza and weather If many people are assembled underneath some antipathetic atmospheric disturbance then many of them will get sick, yes, but there is no spreading and relatives are safe because the causal factor is localised and temporary.
The spread
“If it is a toxin, how do we explain this diagram? Is there evidence that on a certain day that thousands of communities all conspired to release a toxin?”
Influenza is seasonal and travels along latitudes. It has something to do with weather patterns, pressure fronts and downdrafts. It is not inconceivable that toxins accumulate in the air and are concentrated at certain locations.
Other viruses: what are they and why do they match their associated diseases?
No virus has yet been demonstrated and correlation is not causation.
Causation is top down in biological systems and a disease state will lead to very precise changes in the way that RNA is constructed. The drinking of alcohol will alter DNA in a precise fashion, various metabolic patterns can be induced in mice. These traits are codified at the molecular level and passed on to the next generation.
Precise disease states will produce, somehow and for some reason, precise changes in RNA production.
The Washburne paper shows it is HIGHLY unlikely the virus is of natural origin. The genome is consistent with a man-made virus because it has certain genetic fingerprints that have never been found in nature before.
The mere fact of something being man made in no way adds to the likelihood that it is a virus.
The measles virus
“The measles virus is one of the most infectious viruses known to man. An infected person can spread the virus to up to nine out of ten susceptible people who are close contacts.”
Nine out of ten sounds like a lot but it only applies to susceptible people! People who are susceptible get ill – by definition of susceptible!
Again and again: spreading is never directly observed, always assumed. This is why we are in such a mess.
Measles, like many other diseases is seasonal: Seasonal disease. Seasonal and localised incidence has been mistaken for contagion.
Science is about using all available evidence
Yes, so the epidemiology, the seasonality and correlation with the weather, all need some explanation.
The correlation between genome sequences and disease is interesting but is so far just a load of correlations and lack of an explanation does not in any way prove germ theory.