Virus Novelty Myth - Had SARS-COV-2 been truly novel, the disaster would have been far worse than the epidemic that killed most Aztecs following Columbus' landing.
As I commented on your “Lifting the Fog over Decades of Injuries” article, I think you have done an outstanding job in building the bolus theory. In this article, I like how you suggested that children produce fewer infectious virions than adults. I don’t think I have seen other epidemiologists highlight this. I think the rest of your description of immunity in this article also makes good sense, although I was surprised you hardly mention innate immunity, which seems to have a large role in preventing infection in adults as well as children.
I want to challenge you, however, on many of the assumptions you make about transmission of respiratory viruses. Mainstream infectious disease researchers make the same assumptions. I raise these criticisms with you, because you seem to be a free thinker (mainstream researchers, unfortunately, do not think freely).
One key assumption is that all or most transmission of respiratory viruses occurs as a result of close personal contact, shared airspaces, and inhalation of infectious aerosols exhaled by others in those airspaces. An extension of this assumption is that high population density leads to high transmission/infection incidence, and low population density leads to low transmission/incidence, with the intensity, frequency, and extent/scope of social interaction determining how much transmission can occur. I am aware of no _strong_ evidence that respiratory viruses spread in this way. Strong evidence would include, at a minimum, information on contact patterns among infected and uninfected persons, their infection statuses and dates of infection, and the genetic relatedness of infected persons' viral variants. Most epidemiologic research and investigation on infectious disease (of any type) excludes one or more of these components. Of course, other information, such as serological evidence of prior exposure to the pathogen under study, would also be useful. My colleagues and I conducted a study on transmission of hepatitis C virus that included the key components (https://is.gd/4QYomkq). There are very few similar studies for other infections. If you know of any for respiratory viruses, please let me know.
Likewise, there is not a consistent association between population density and infection/illness incidence. For instance, consider this lack of association for influenza: https://onlinelibrary.wiley.com/doi/full/10.1111/irv.13032. Of course, others have reported an association, but population density is confounded by many factors that are associated with immunity to respiratory infections. My point is that epidemiologists assume (especially in modeling exercises) that population density is a factor driving transmission, without a good empirical basis for this assumption.
Apart from the lack of good evidence for the mainstream belief about how respiratory viruses spread, there are some critical observations that mainstream epidemiologists have not explained, in my opinion. For example, even before air travel and rapid overland/sea transport, influenza epidemics were synchronized in temperate regions separated by oceans and large expanses of continents. Likewise, as the world has become more thoroughly connected with high speed transport, the transmission of respiratory viruses has not increased accordingly (or at all), as far as I am aware. Also, there have been repeated reports of respiratory viral illness outbreaks in groups/communities of previously healthy persons who had not been in any contact with infected persons for periods much longer than the incubation/latency periods of the viruses involved (such as ocean ship crews and Antarctic station crews). Another related empirical challenge is to account for where respiratory viruses go after an epidemic and from where do they come before an epidemic. This applies especially to viruses that are persistent from year to year (as opposed to new viruses that might emerge from other species). How do respiratory viruses, with their fairly short incubation and symptomatic periods, endure? They have to be reproducing constantly somewhere in the world and there must be some sort of bridge that allows an epidemic to spread from one area to another perpetually.
Some possible alternate explanations of such events – and for transmission of respiratory viruses generally -- are the atmospheric distribution and deposition of infectious aerosols/particulates, environmental contamination with and long-term viability of viral material; and latent reservoirs of virus within individuals' bodies that somehow evade their immune systems and later develop into active infections when their immunity drops (such as in response to a seasonal decline in serum vitamin D). As far as I know, researchers have not evaluated any of these hypotheses in rigorous studies, so that puts them on equal footing with the mainstream hypothesis of how transmission occurs. It’s possible that many or all of these mechanisms (and others, including the mainstream hypothesis) could be involved with transmission.
In many ways, transmission of respiratory viruses is like adverse effects from vaccines. Researchers have assumed, without good evidence, the underlying mechanisms, and this may lead to wrong conclusions about prevention. You looked at adverse effects from vaccines with a fresh perspective and the result is a possible huge advance in understanding and prevention.
You should aim higher. Instead of being a COVID Myth Buster, you should be a virus myth buster. For the science, superbly well explained, start here: https://odysee.com/@TruthVault:0/The-End-of-Germ-Theory:b It's 2 1/2 hours, but the first 90 minutes will give you the bulk of what you need to know, and you can play it at 1.25 speed.
I don't believe Noble savages were killed by viruses - I think that is a convenient lie to cover the fact that the invaders brought not viruses but alcohol and guns with which they massacred indigenous people and stole their land.
A lot of people were vilified for saying CV-19 was no worse than the flu. It isn't any worse. How many people would the regular flu kill if no one had any immunity to it? What if no one even had a previous upper respiratory infection remotely related to it? It would look exactly like CV-19. As time goes on, its variants will become the new colds and flu. We are probably fast approaching the point where, like the regular flu, an infection is very unlikely to be fatal unless one happens to be in a very vulnerable state due to advanced age or disease. The rationale for taking the vax goes down rapidly from here. And since we now know it does not stop transmission, getting the jab should be completely up to the individual and no longer a public health concern.
You need to get more basic in your myth busting, meaning you need to study how the DNA sequence was determined. Christian Drosten's team published the paper and the sequence--the sequence which the entire world depended on to formulate their PCR tests. In the paper it was stated that no sample of the virus was available!! In other words, they and their computer just made it up.
Without a DNA sequence, the PCR test is meaningless; it tells you nothing.
Furthermore, any variants are similarly fictional.
The only conclusion is that the entire operation was a purposeful hoax.
Novel does not mean dangerous. There are probably hundreds of novel viruses jumping from other species but are too mild so we don't even have a name for them. Only when a virus kills enough to gain attention like SARS-CoV-2, we name it and start analyzing it.
Immunological Mechanisms Explaining the Role of Vaccines, IgE, Mast Cells, Histamine, Elevating Ferritin, IL-6, D-dimer, VEGF Levels in COVID-19 and Dengue, Potential Treatments Such as Mast Cell Stabilizers, Antihistamines: Predictions and Confirmations
I a have zero qualifications just a guy on the internet with an interest in this. Here is a hypothesis to challenge. What if the Spike Protein is really what is spreading meaning it was originally attached to a virus in the labs, and once in the wild the spike proteins attached themselves to flu viruses or common cold (corona viruses) etc through the vaccines or regular infection and the test merely picked up some of the genes from the spike protein? . So everything is covid and the "variants" are the spike attaching to other viruses? Would answer a lot of mysteries like where did the flu and common cold go?
Thank you for this series. I always come away from your articles feeling like I have learned something new and useful. You have a great way of explaining to those of us who don't have deep science backgrounds. Very much worth the time to read all three sections.
I wrote this in late 2021 (at the time, the IFR was thought to be somewhere in the neighborhood of 0.15% to 0.24%):
COVID has an infection fatality rate of well under 1%. You could say another variant might be worse, but because the bar to becoming "worse" is so low, even if the IFR were to double, it would still be under 1%.
On the other hand, with a survival rate of over 99%, it's difficult to imagine how the survival rate could improve. The survival rate is so good, that there is only room for an improvement of a tenth or two of one percent.
This what all the sturm und drang is about, increasing the survival rate a few tenths of a percent? Stamping out a disease with a survival rate so good that it's nearly impossible to improve, and an IFR that's so low that it's easier to imagine it doubling than it is to imagine it getting lower?
This was an informative and extensive article that lays out much of what some of us have known, but I’m especially impressed how you balanced science with logic.
As I commented on your “Lifting the Fog over Decades of Injuries” article, I think you have done an outstanding job in building the bolus theory. In this article, I like how you suggested that children produce fewer infectious virions than adults. I don’t think I have seen other epidemiologists highlight this. I think the rest of your description of immunity in this article also makes good sense, although I was surprised you hardly mention innate immunity, which seems to have a large role in preventing infection in adults as well as children.
I want to challenge you, however, on many of the assumptions you make about transmission of respiratory viruses. Mainstream infectious disease researchers make the same assumptions. I raise these criticisms with you, because you seem to be a free thinker (mainstream researchers, unfortunately, do not think freely).
One key assumption is that all or most transmission of respiratory viruses occurs as a result of close personal contact, shared airspaces, and inhalation of infectious aerosols exhaled by others in those airspaces. An extension of this assumption is that high population density leads to high transmission/infection incidence, and low population density leads to low transmission/incidence, with the intensity, frequency, and extent/scope of social interaction determining how much transmission can occur. I am aware of no _strong_ evidence that respiratory viruses spread in this way. Strong evidence would include, at a minimum, information on contact patterns among infected and uninfected persons, their infection statuses and dates of infection, and the genetic relatedness of infected persons' viral variants. Most epidemiologic research and investigation on infectious disease (of any type) excludes one or more of these components. Of course, other information, such as serological evidence of prior exposure to the pathogen under study, would also be useful. My colleagues and I conducted a study on transmission of hepatitis C virus that included the key components (https://is.gd/4QYomkq). There are very few similar studies for other infections. If you know of any for respiratory viruses, please let me know.
Likewise, there is not a consistent association between population density and infection/illness incidence. For instance, consider this lack of association for influenza: https://onlinelibrary.wiley.com/doi/full/10.1111/irv.13032. Of course, others have reported an association, but population density is confounded by many factors that are associated with immunity to respiratory infections. My point is that epidemiologists assume (especially in modeling exercises) that population density is a factor driving transmission, without a good empirical basis for this assumption.
Apart from the lack of good evidence for the mainstream belief about how respiratory viruses spread, there are some critical observations that mainstream epidemiologists have not explained, in my opinion. For example, even before air travel and rapid overland/sea transport, influenza epidemics were synchronized in temperate regions separated by oceans and large expanses of continents. Likewise, as the world has become more thoroughly connected with high speed transport, the transmission of respiratory viruses has not increased accordingly (or at all), as far as I am aware. Also, there have been repeated reports of respiratory viral illness outbreaks in groups/communities of previously healthy persons who had not been in any contact with infected persons for periods much longer than the incubation/latency periods of the viruses involved (such as ocean ship crews and Antarctic station crews). Another related empirical challenge is to account for where respiratory viruses go after an epidemic and from where do they come before an epidemic. This applies especially to viruses that are persistent from year to year (as opposed to new viruses that might emerge from other species). How do respiratory viruses, with their fairly short incubation and symptomatic periods, endure? They have to be reproducing constantly somewhere in the world and there must be some sort of bridge that allows an epidemic to spread from one area to another perpetually.
Some possible alternate explanations of such events – and for transmission of respiratory viruses generally -- are the atmospheric distribution and deposition of infectious aerosols/particulates, environmental contamination with and long-term viability of viral material; and latent reservoirs of virus within individuals' bodies that somehow evade their immune systems and later develop into active infections when their immunity drops (such as in response to a seasonal decline in serum vitamin D). As far as I know, researchers have not evaluated any of these hypotheses in rigorous studies, so that puts them on equal footing with the mainstream hypothesis of how transmission occurs. It’s possible that many or all of these mechanisms (and others, including the mainstream hypothesis) could be involved with transmission.
In many ways, transmission of respiratory viruses is like adverse effects from vaccines. Researchers have assumed, without good evidence, the underlying mechanisms, and this may lead to wrong conclusions about prevention. You looked at adverse effects from vaccines with a fresh perspective and the result is a possible huge advance in understanding and prevention.
"why did we mistreated our kids, destroyed our economies, injected billions with ineffective - sometimes dangerous - vaccines, ..."
After some reflection it becomes obvious.
https://peterwebster.substack.com/p/vaxscam?s=w
All other motives, reasons, plans, are just successive layers on top of the fundamental one.
https://research.com/u/didier-raoult
H-index 175
You should aim higher. Instead of being a COVID Myth Buster, you should be a virus myth buster. For the science, superbly well explained, start here: https://odysee.com/@TruthVault:0/The-End-of-Germ-Theory:b It's 2 1/2 hours, but the first 90 minutes will give you the bulk of what you need to know, and you can play it at 1.25 speed.
Hi,
I don't believe Noble savages were killed by viruses - I think that is a convenient lie to cover the fact that the invaders brought not viruses but alcohol and guns with which they massacred indigenous people and stole their land.
There is no evidence that any virus exists or causes disease https://georgiedonny.substack.com/p/seeing-is-believing
A lot of people were vilified for saying CV-19 was no worse than the flu. It isn't any worse. How many people would the regular flu kill if no one had any immunity to it? What if no one even had a previous upper respiratory infection remotely related to it? It would look exactly like CV-19. As time goes on, its variants will become the new colds and flu. We are probably fast approaching the point where, like the regular flu, an infection is very unlikely to be fatal unless one happens to be in a very vulnerable state due to advanced age or disease. The rationale for taking the vax goes down rapidly from here. And since we now know it does not stop transmission, getting the jab should be completely up to the individual and no longer a public health concern.
They took a nasty flu and gave us a poisonous vax. This was never about health. The NIH and CDC should be leveled
You need to get more basic in your myth busting, meaning you need to study how the DNA sequence was determined. Christian Drosten's team published the paper and the sequence--the sequence which the entire world depended on to formulate their PCR tests. In the paper it was stated that no sample of the virus was available!! In other words, they and their computer just made it up.
Without a DNA sequence, the PCR test is meaningless; it tells you nothing.
Furthermore, any variants are similarly fictional.
The only conclusion is that the entire operation was a purposeful hoax.
Novel does not mean dangerous. There are probably hundreds of novel viruses jumping from other species but are too mild so we don't even have a name for them. Only when a virus kills enough to gain attention like SARS-CoV-2, we name it and start analyzing it.
Immunological Mechanisms Explaining the Role of Vaccines, IgE, Mast Cells, Histamine, Elevating Ferritin, IL-6, D-dimer, VEGF Levels in COVID-19 and Dengue, Potential Treatments Such as Mast Cell Stabilizers, Antihistamines: Predictions and Confirmations
https://europepmc.org/article/PPR/PPR241819#R15
I a have zero qualifications just a guy on the internet with an interest in this. Here is a hypothesis to challenge. What if the Spike Protein is really what is spreading meaning it was originally attached to a virus in the labs, and once in the wild the spike proteins attached themselves to flu viruses or common cold (corona viruses) etc through the vaccines or regular infection and the test merely picked up some of the genes from the spike protein? . So everything is covid and the "variants" are the spike attaching to other viruses? Would answer a lot of mysteries like where did the flu and common cold go?
Thank you for this series. I always come away from your articles feeling like I have learned something new and useful. You have a great way of explaining to those of us who don't have deep science backgrounds. Very much worth the time to read all three sections.
A very worthy read! Thank you!
"Novel coronavirus" is an oxymoron. Nuff said.
I wrote this in late 2021 (at the time, the IFR was thought to be somewhere in the neighborhood of 0.15% to 0.24%):
COVID has an infection fatality rate of well under 1%. You could say another variant might be worse, but because the bar to becoming "worse" is so low, even if the IFR were to double, it would still be under 1%.
On the other hand, with a survival rate of over 99%, it's difficult to imagine how the survival rate could improve. The survival rate is so good, that there is only room for an improvement of a tenth or two of one percent.
This what all the sturm und drang is about, increasing the survival rate a few tenths of a percent? Stamping out a disease with a survival rate so good that it's nearly impossible to improve, and an IFR that's so low that it's easier to imagine it doubling than it is to imagine it getting lower?
This was an informative and extensive article that lays out much of what some of us have known, but I’m especially impressed how you balanced science with logic.
Masterful writing! As insightful as anything I have read on Covid! Thank You!