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.
That's a lot to answer to, and I don't know I have the time to answer to it all.
A few points:
- There's no doubt in my mind that viruses are everywhere and that we are surrounded by them all year long. we fight them off, as they try to reproduce here and there, all year. When winter arrives - or too hot a summer - we get back in-doors and the doses we expel are much more concentrated, and repeated, and so have a higher probability to make us sick. Even someone with sterilising immunity can be the host and replicate some virions for a few hours. Infection is continuous, not discrete, in my view.
- lived population density is obviously part of the equation: more hosts to produce virions and more targets to infect in the same space is a mathematical certainty. The mucosal immunity messes with the true incidence, apparent incidence is an illusion. Read my article on NY, we thought 13% had been contaminated by SC2, when 83% had been infected but with 70% asymptomatic. What counts is reducing areas with poisonous doses...hospitals, care homes.
-Just like I am more and more convinced Hepatis virus can possibly be harmful injected as a bolus, but not with natural infection for healthy people. I just don't see how the infection/reaction ratio would be in favour of the virus if only a small 2D portion is susceptible to infection while dendritic cells have the entire body in a 3D to meet the virus, and react. The odds are too much against the virus. See how children hardly are touched by the virus, with only 20% less ACE-2.
Thank you for your thoughts, Marc. You've introduced an interesting additional hypothesis: that viruses that cause seasonal respiratory infections persist year-round even in temperate climates. I think that there is essentially no evidence for this hypothesis. The corresponding illnesses and detected infections do seem to disappear for months at a time, and they don't seem to be detectable in the environment continuously throughout the year. Or do you know of evidence of such persistence?
I think your view of infection on a continuum makes sense. However, can the very low hypothetical viral replication in a person with sterilizing immunity be the basis for sustained transmission, enough to prevent local extinction of the virus?
I don't have the same faith in SC2 diagnostics that you do, so I don't try to make sense of results based on them. Ecological analyses (such as at the country level) have many kinds of confounding factors, and they are often very difficult to interpret well.
Could you please explain further what you meant about hepatitis virus? I don't follow your last paragraph.
- On continuity, only stimulated mucosal immunity remains. When you look at the Stockhölm (pre-Covid tonsils) and Yokohama (dentistry University) studies, you get 50+% have mucosal immunity with IgA or resident T-cells that means the virus is still in the environment. Else the immunity would wane like in less dense areas like Norway.
- I don't understand how a virus can hit only one specific organ. If the receptor is universal like SC2, you end up with a Cytokine storm for those who are immune compromised (see the Israeli study showing no myocarditis for COVID). For viruses that are organ specific, the reaction time is inevitably the same as the virions circulate the body and meet the same number of dendritic cells.
And so, on those grounds, only immunocompromised, junkies (bolus of virus injected) or vaccine injured can suffer from hepatitis. This would mean all the vaccines are utterly useless. I always believed polio was real, I am not sure anymore...
Your thoughts about organ-specific viruses are interesting, and I hadn't considered that before.
For hepatitis B, I think most of the hepatitis occurs in individuals infected as children (usually infancy, if I recall correctly). Adult infections, even in drug injectors, rarely lead to hepatitis. Hepatitis C is different, though, and almost any persistent HCV infection comes from what you would call a bolus (lower level exposures to HCV and HIV sometimes produce short-lived transient infections without seroconversion). And I agree that many diseases may not be what doctors and epidemiologists have told us they are (such as polio, scurvy, and others).
Thank you, Marc. I will try to find the Stockholm and Yokohama studies. I appreciate your creative hypothesizing. You have framed this viral persistence hypothesis as individuals continuing to get infected (briefly and at low levels) and transmitting (presumably also at very low levels), all without illness in the "off" season (such as summer in temperate climates). I still wonder whether that's a viable process for persistence. Another possibility is long-term viability of a virus in the environment. In this view, the virus reproduces on a massive scale during the illness season (viremia and the efficient distribution mechanisms of coughing and sneezing). Most of the virions expelled into the environment would become non-viable over time, but perhaps it's a probability game. It could be that some small fraction remains viable, and that incidental exposures (e.g., to dust in homes) keep the mucosal immunity current in many individuals in the off-season, and then lead to illness in others with seasonal declines in innate immunity (driven by falling serum vitamin D and perhaps other factors) as the process begins again in illness season.
In any event, your hypothesis is another fundamental challenge to mainstream epidemiology, but this time with respect to respiratory virus transmission. The mainstream presents transmission as a seasonal stream that spreads across the world. Your hypothesis would also account for the transmission anomalies I mentioned originally.
Thank you, Marc. Travel might be correlated with seasonal pandemics, but it also might not be causally related. Both it and the alternative hypotheses I mentioned have not been tested rigorously (to the exclusion of the others), as far as I know. Do you know of any strong evidence? And travel doesn't account for synchronized epidemics before high speed transport.
The articles you mentioned don't seem to have any information about the duration of mucosal immunity. If I understand you correctly, you interpret detectable mucosal immunity as indicating recent exposure that fades quickly (in weeks or months, but less than a year). I did a quick and very incomplete search, but couldn't find other sources on the duration of mucosal immunity.
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.
Right you are, g&d. The virus misconception is deep in the public's psyche, however, and truth will require will decades to overcome that myth. The billions and trillions of $$$ being collected by Big Pharma from that fraud will make it even harder.
Incidentally, another explanation on the noble savages is that the settlers provided them blankets, many of which (unknowingly) had bedbugs. Allergic reactions to bedbug bites have been claimed by certain knowledgeable researchers to be the actual cause of smallpox.
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.
Unfortunately, it is very probable other transfecting vax are as lethal (smallpox, chickenpox, MMR, yellow fever,...) when injected intravenous by accident.
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.
Do you have a link to the paper where he explains how it was done? No person or government entity has been able to find one. In fact, over 150 governmental health entities from all over the world are on record specifically denying that they have been able to find such a paper.
to your statement that "Professor Raoult in Marseille have sequenced the virus multiple times and seen tits evolution...". In response your link is months old NON-PEER REVIEW paper asserting pangolin lineage variants that are categorically NOT Sars CoV2. And are assuredly not the genomes used ANYWHERE
as PCR assays to detect viral fragments. That pre-print is useless in the cause of asserting the existence of CoV2.
Really? What's his score? Where can we view the "best micro-biologists" leaderboard?
I didn't subscribe to be adversarial but every comment you make takes your credibility down. You are the one not relying on science or facts. Asymptomatic transmission was not a driver of infection. Period. That illusion, created to reinforce the fear to drive compliance, was only supported by the PCR fraud.
The paper you posted by Mr Best Microbiologist actually refers to pangolin lineage whereas pangolins were ruled out due
to not being physically proximal to Wuhan. The timing of the paper as Dec 2021 renders it moot as well. Not to mention that it is not peer reviewed.
Any alleged sequencing of Sars-CoV2 would have to have been done by Jan 2020 otherwise that is moot to the isolation question and development of assay panels deployed the world over to claim a case thereby shutting down entire societies. Confirming of 2021-2022 alleged isolates using PCR assays of the-never-isolated-non-existent-novel-virus using admittedly CONTRIVED SYNTHETIC genomic assays from 2020 AND THEN overclocking the
Marc, The paper that you linked suffers from the same fundamental lack of science that infects so much of SARS-COV-2 analysis (and indeed all of virology). The virus itself has never been isolated, even though doing so is absolutely essential to determining its DNA sequence and a complete DNA sequence is absolutely essential to having a useful PCR test. Read the Corman-Drosten paper which provided the supposed sequence to the world and you’ll find they did not even try to isolate the virus. It admits to having no virus material available. This isn’t science, it’s blatant fraud. Your friend Kevin McKernan is familiar with the gross incompetence of Corman-Drosten and has co-authored a paper on it:
So you assert a Dec 21 paper details sequencing of the highly mutagenic CoV2 from which the PCR tests were based 1 year earlier? And that supports the billions of PCR frauds from the beginning before this sequencing?
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
It all depends what you believe drives pathogenicity.
Indeed a novel virus with slow replication capability will give time enough to the immune system to react. But a novel virus with faster replication capability can drive high propagation, daunting high inocula network effects that would cause repeated poisonous inocula in a community. Despite its rapid reproduction this didn't happen bc so many pple had sterilising immunity already.
We have to explain why COVID is harmful to only some. As I explain above, it is due to vaccine damage from traditional vaccines. The human immune system (undamaged) has evolved to deal with novel viruses.
Undeniable that the term novel was weaponized to stoke the fear. Furthermore it continues to be used as a shield for experts to use as cover for their claims of not knowing any number of previously immutable tenets of immunology
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.
Believe me, I have suggested your Substack page to many people. Some I sadly believe just simply don't want to hear or read anything that deviates from the prescribed narrative. Others prefer to listen to sound-bites rather than read. Because none of what the so-called Public Health experts have advocated since early 2020 has made a lick of sense to me, I prefer to read more than listen, and have bookmarked more articles and studies than you can imagine. I really appreciate your writing because it is clear that your motive is education more than anything else. I will always take the time to read what you post on Substack, and have never come away thinking I had wasted my time.
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.
That's a lot to answer to, and I don't know I have the time to answer to it all.
A few points:
- There's no doubt in my mind that viruses are everywhere and that we are surrounded by them all year long. we fight them off, as they try to reproduce here and there, all year. When winter arrives - or too hot a summer - we get back in-doors and the doses we expel are much more concentrated, and repeated, and so have a higher probability to make us sick. Even someone with sterilising immunity can be the host and replicate some virions for a few hours. Infection is continuous, not discrete, in my view.
- lived population density is obviously part of the equation: more hosts to produce virions and more targets to infect in the same space is a mathematical certainty. The mucosal immunity messes with the true incidence, apparent incidence is an illusion. Read my article on NY, we thought 13% had been contaminated by SC2, when 83% had been infected but with 70% asymptomatic. What counts is reducing areas with poisonous doses...hospitals, care homes.
Check these graphs: https://twitter.com/GirardotMarc/status/1352725473567121417
https://twitter.com/GirardotMarc/status/1349425816640303106
-Just like I am more and more convinced Hepatis virus can possibly be harmful injected as a bolus, but not with natural infection for healthy people. I just don't see how the infection/reaction ratio would be in favour of the virus if only a small 2D portion is susceptible to infection while dendritic cells have the entire body in a 3D to meet the virus, and react. The odds are too much against the virus. See how children hardly are touched by the virus, with only 20% less ACE-2.
Thank you for your thoughts, Marc. You've introduced an interesting additional hypothesis: that viruses that cause seasonal respiratory infections persist year-round even in temperate climates. I think that there is essentially no evidence for this hypothesis. The corresponding illnesses and detected infections do seem to disappear for months at a time, and they don't seem to be detectable in the environment continuously throughout the year. Or do you know of evidence of such persistence?
I think your view of infection on a continuum makes sense. However, can the very low hypothetical viral replication in a person with sterilizing immunity be the basis for sustained transmission, enough to prevent local extinction of the virus?
I don't have the same faith in SC2 diagnostics that you do, so I don't try to make sense of results based on them. Ecological analyses (such as at the country level) have many kinds of confounding factors, and they are often very difficult to interpret well.
Could you please explain further what you meant about hepatitis virus? I don't follow your last paragraph.
- On continuity, only stimulated mucosal immunity remains. When you look at the Stockhölm (pre-Covid tonsils) and Yokohama (dentistry University) studies, you get 50+% have mucosal immunity with IgA or resident T-cells that means the virus is still in the environment. Else the immunity would wane like in less dense areas like Norway.
- I don't understand how a virus can hit only one specific organ. If the receptor is universal like SC2, you end up with a Cytokine storm for those who are immune compromised (see the Israeli study showing no myocarditis for COVID). For viruses that are organ specific, the reaction time is inevitably the same as the virions circulate the body and meet the same number of dendritic cells.
And so, on those grounds, only immunocompromised, junkies (bolus of virus injected) or vaccine injured can suffer from hepatitis. This would mean all the vaccines are utterly useless. I always believed polio was real, I am not sure anymore...
Your thoughts about organ-specific viruses are interesting, and I hadn't considered that before.
For hepatitis B, I think most of the hepatitis occurs in individuals infected as children (usually infancy, if I recall correctly). Adult infections, even in drug injectors, rarely lead to hepatitis. Hepatitis C is different, though, and almost any persistent HCV infection comes from what you would call a bolus (lower level exposures to HCV and HIV sometimes produce short-lived transient infections without seroconversion). And I agree that many diseases may not be what doctors and epidemiologists have told us they are (such as polio, scurvy, and others).
Thank you, Marc. I will try to find the Stockholm and Yokohama studies. I appreciate your creative hypothesizing. You have framed this viral persistence hypothesis as individuals continuing to get infected (briefly and at low levels) and transmitting (presumably also at very low levels), all without illness in the "off" season (such as summer in temperate climates). I still wonder whether that's a viable process for persistence. Another possibility is long-term viability of a virus in the environment. In this view, the virus reproduces on a massive scale during the illness season (viremia and the efficient distribution mechanisms of coughing and sneezing). Most of the virions expelled into the environment would become non-viable over time, but perhaps it's a probability game. It could be that some small fraction remains viable, and that incidental exposures (e.g., to dust in homes) keep the mucosal immunity current in many individuals in the off-season, and then lead to illness in others with seasonal declines in innate immunity (driven by falling serum vitamin D and perhaps other factors) as the process begins again in illness season.
In any event, your hypothesis is another fundamental challenge to mainstream epidemiology, but this time with respect to respiratory virus transmission. The mainstream presents transmission as a seasonal stream that spreads across the world. Your hypothesis would also account for the transmission anomalies I mentioned originally.
Kanagawa Dentistry University:
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0249979
Karolinska Institutet:
https://www.science.org/doi/full/10.1126/sciimmunol.abk0894
It's obvious that travel also contributes to reigniting and fueling seasonal pandemics.
Thank you, Marc. Travel might be correlated with seasonal pandemics, but it also might not be causally related. Both it and the alternative hypotheses I mentioned have not been tested rigorously (to the exclusion of the others), as far as I know. Do you know of any strong evidence? And travel doesn't account for synchronized epidemics before high speed transport.
The articles you mentioned don't seem to have any information about the duration of mucosal immunity. If I understand you correctly, you interpret detectable mucosal immunity as indicating recent exposure that fades quickly (in weeks or months, but less than a year). I did a quick and very incomplete search, but couldn't find other sources on the duration of mucosal immunity.
"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.
amazing video work, thanks for link
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
Right you are, g&d. The virus misconception is deep in the public's psyche, however, and truth will require will decades to overcome that myth. The billions and trillions of $$$ being collected by Big Pharma from that fraud will make it even harder.
Incidentally, another explanation on the noble savages is that the settlers provided them blankets, many of which (unknowingly) had bedbugs. Allergic reactions to bedbug bites have been claimed by certain knowledgeable researchers to be the actual cause of smallpox.
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
Unfortunately, it is very probable other transfecting vax are as lethal (smallpox, chickenpox, MMR, yellow fever,...) when injected intravenous by accident.
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.
My understanding is the Professor Raoult in Marseille have sequenced the virus multiple times and seen tits evolution...
Do you have a link to the paper where he explains how it was done? No person or government entity has been able to find one. In fact, over 150 governmental health entities from all over the world are on record specifically denying that they have been able to find such a paper.
https://www.medrxiv.org/content/10.1101/2021.12.24.21268174.abstract
Bubblehead asked for a link from you in response
to your statement that "Professor Raoult in Marseille have sequenced the virus multiple times and seen tits evolution...". In response your link is months old NON-PEER REVIEW paper asserting pangolin lineage variants that are categorically NOT Sars CoV2. And are assuredly not the genomes used ANYWHERE
as PCR assays to detect viral fragments. That pre-print is useless in the cause of asserting the existence of CoV2.
Pr Raoult is one of the best micro-biologists.
Please being forth scientific facts and arguments if you disagree. Deconstructing is easy. Respectfully
Really? What's his score? Where can we view the "best micro-biologists" leaderboard?
I didn't subscribe to be adversarial but every comment you make takes your credibility down. You are the one not relying on science or facts. Asymptomatic transmission was not a driver of infection. Period. That illusion, created to reinforce the fear to drive compliance, was only supported by the PCR fraud.
The paper you posted by Mr Best Microbiologist actually refers to pangolin lineage whereas pangolins were ruled out due
to not being physically proximal to Wuhan. The timing of the paper as Dec 2021 renders it moot as well. Not to mention that it is not peer reviewed.
Any alleged sequencing of Sars-CoV2 would have to have been done by Jan 2020 otherwise that is moot to the isolation question and development of assay panels deployed the world over to claim a case thereby shutting down entire societies. Confirming of 2021-2022 alleged isolates using PCR assays of the-never-isolated-non-existent-novel-virus using admittedly CONTRIVED SYNTHETIC genomic assays from 2020 AND THEN overclocking the
test off the charts proves absolutely nothing.
Marc, The paper that you linked suffers from the same fundamental lack of science that infects so much of SARS-COV-2 analysis (and indeed all of virology). The virus itself has never been isolated, even though doing so is absolutely essential to determining its DNA sequence and a complete DNA sequence is absolutely essential to having a useful PCR test. Read the Corman-Drosten paper which provided the supposed sequence to the world and you’ll find they did not even try to isolate the virus. It admits to having no virus material available. This isn’t science, it’s blatant fraud. Your friend Kevin McKernan is familiar with the gross incompetence of Corman-Drosten and has co-authored a paper on it:
https://www.medicdebate.org/node/1183
So you assert a Dec 21 paper details sequencing of the highly mutagenic CoV2 from which the PCR tests were based 1 year earlier? And that supports the billions of PCR frauds from the beginning before this sequencing?
C'mon man. The logical fallacy is astounding!
I am not asserting anything. You asked me for a paper. I gave you one from one. Sequencing is not based on PCR test.
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
It all depends what you believe drives pathogenicity.
Indeed a novel virus with slow replication capability will give time enough to the immune system to react. But a novel virus with faster replication capability can drive high propagation, daunting high inocula network effects that would cause repeated poisonous inocula in a community. Despite its rapid reproduction this didn't happen bc so many pple had sterilising immunity already.
We have to explain why COVID is harmful to only some. As I explain above, it is due to vaccine damage from traditional vaccines. The human immune system (undamaged) has evolved to deal with novel viruses.
Undeniable that the term novel was weaponized to stoke the fear. Furthermore it continues to be used as a shield for experts to use as cover for their claims of not knowing any number of previously immutable tenets of immunology
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.
Thank you Victoria... A lot of thinking at night these past 2 years. Feel free to circulate my articles. Can't say my messages are getting out...
Believe me, I have suggested your Substack page to many people. Some I sadly believe just simply don't want to hear or read anything that deviates from the prescribed narrative. Others prefer to listen to sound-bites rather than read. Because none of what the so-called Public Health experts have advocated since early 2020 has made a lick of sense to me, I prefer to read more than listen, and have bookmarked more articles and studies than you can imagine. I really appreciate your writing because it is clear that your motive is education more than anything else. I will always take the time to read what you post on Substack, and have never come away thinking I had wasted my time.
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.
Thank you Ely very appreciative of your kind comment!
Masterful writing! As insightful as anything I have read on Covid! Thank You!