What everyone seems to ignore is the fact that the source of both COVID-19 and the mRNA injection are from the same group  that are trying to build profit and reduce world population. Both contain the same spike protein just in different quantities. As Tennessee Ernie Ford used to sing if the first one don’t get you the second one will.
Boy, I wish I had this available about a year ago when arguing with a med student on the efficacy of masks against viruses. He stated the fact that flu had disappeared during covid was proof masks worked against viruses. Ignoring for the moment that if they worked against the flu so well that it disappeared, why then is covid still spreading, I brought up this condition you describe of one infectious agent suppressing others. The med student said I didn’t know what I was talking about, that no such thing exists.
Not to take away from your excellent research, but it's "toe the line", not "tow the line". It comes from holding a footrace, and "toeing" the starting line. ;-)
Stephen the "seasonal signal" that Hope-Simpson was looking for is almost certainly just temperature.
Respiratory viruses need to keep out of our lungs/sinuses etc, in order to keep us moving around. They (almost all) seem to do this by sensing temperature - they are more active below the normal body temperature of their host.
What Hope-Simpson didn't get is that resp viruses adapt to their local climate and season in a few months by gaining or losing thermal sensitivity. They have to lose thermal sensitivity in the Tropics in order to replicate at all. In cold regions nearer the poles they have to gain thermal sensitivity to stop us going to bed very quickly with a fever and not spreading the virus much.
CoV-2 (and influenza etc) is thermally sensitive in the wet-lab and in animals:
I do not know whether you have had a chance to look at any of my other substack articles? This one provides experimental evidence on the ability of uv light to facilitate covid-19 cell entry;
I do know Hope-Simpson's work very well. As I mentioned, what he didn't get is that pretty well all respiratory viruses are thermally-sensitive (more active below normal body temp of their host), but they have to adapt their thermal sensitivity to their local climate and season. This takes a few months.
I'm not sure of the details of your hypothesis, but I have several comments
1. Colds and flu don't follow cloudy weather, and are not suppressed by sunny weather. They follow COLD weather. There are many refs for this - see our review - but a good one is Lidwell
Lidwell, O., Morgan, R., & Williams, R. (1965). The epidemiology of the common cold IV. The effect of weather. Journal of Hygiene, 63(3), 427-439. doi:10.1017/S0022172400045319
2. Colds and flu persist at intermediate levels year-round in the Tropics. This is because strains there lose their thermal sensitivity - because they have to. This explains why eg flu tends to go from hot places to colder (see figure 14 in our review)
3. Most transmission takes place indoors. The amount of time we spend indoors varies by only about 1 hour between summer and winter. (The amount of time we spend outdoors varies a lot, but so what?)
4. In any case I think this argument is settled by the observation that CoV-2 is thermally sensitive in the wet-lab and in animals: https://doi.org/10.1016/j.imj.2022.08.005
We cite 7 papers in our letter, but there are more.
I'll read the papers you cite - I haven't seen them all.
This is from one of my Substack articles. Hopefully it expands on the concept. The paper I sent you is just further experimental evidence on the impact of UV light to facilitate cell entry;
The control and regulation of the latent / lysogenic cycles and the movement to the lytic cycles are the key to successful replication of the covid-19 virus. The virus mutates during the lysogenic cycle due to errors in replication. It is proposed that covid-19 initially circulated within a high proportion of the global population at a low level but highly transmissible state and during this phase only mild illness was experienced in the majority of infected individuals. During this infection period a degrees of specific immunity were developed to the prevailing variant(s) in the population. Through a phenomena called quorum sensing (1)(2)(3)(4) the virus has the ability to detect infected host cell availability through chemical signals that have the capability to regulate the lytic infection cycle. A second mechanism of cycle regulation involves highly specific conditions of ultraviolet (UV) light that exist at different times of the day and seasonally. The virus is being continually exhaled by infected individuals at a low level and the viral particles are being modified by the specific conditions of UV light. The modification could involve specific cleavage of the virus into smaller fragments. A proportion of these viral fragments are inhaled by the host, due to the proximity to their own breath. The concentration of these fragments have the capability to act as a feedback signal that a successful variant has escaped the immune system and also conditions are more favourable for external existence and therefore transmission. The movement from the lysogenic to the lytic cycle will be accelerated on the basis of the concentration and specificity of these fragments. The product of both of these continuous feedback cycles reach a threshold level and the selected mutated state of the virus moves to an intense lytic phase releasing favourable mutations and infecting further individuals with potentially more vulnerable immune systems. The seasonally /UV activated period of high infectivity is relatively brief as the reactivated individuals immune system responds to the “high level” lytic cycle challenge. Those individuals exposed to the “new” mutation(s) who mount a more severe immune response do not have a sufficient “new” viral load to be significantly infectious. The release of the selected mutation results in a more serious impact on less healthy immune systems with particular emphasis on the aged through immunosenescence. The overall goal of these two feedback mechanisms is to facilitate successful replication of the virus in the ongoing battle with the host’s immune systems. The emergence of successful variants such as Alpha, Delta and Omicron are a product of this selection process. A high proportion of individuals have immunity from prior coronovirus infections and, depending on the prevalent mutation, not susceptible to infection from that specific mutation. They may be carrying the virus in a latent / lysogenic mutating form but their immune system will resist viral escape and therefore will be receiving a limited feedback chemical signal to increase replication or move to an intense lytic cycle.
Thanks for engaging in a dialogue which has been sadly missing during this whole covid-19 debacle.
It is pretty simple really. UV light is high energy. It will be correlated with temperature. It is almost a perfect fit for Hope-Simpson's proposition's. I have never had anyone challenge this thinking.
Does "pathogenic interference" counter allegations that the March 2020 changes in disease reporting protocols allowed central planners to "muscle out" other seasonal respiratory illnesses and propel the novel virus, lockdown narrative?
Without commenting on your analysis, which seems excellent, I want to make another point. This point seems more and more unassailable to me, as the days since the advent of the Great Covid Dumpster Fire go by. How the absolute freaking hell did the B.S. that is mistaken for public health succeed for so long, when there are people like you and so many others, including Joel, out here to show the folly? I realize the scam runs deep, but seriously, Dr. Fauci is a moron compared to many folks writing on Substack. Are we, as a species, that stupid? (Don't answer that!)
"The chemical signalling that exists between viruses, hosts and bacteria have been known for very many years (7). This was ignored during the pandemic. If you are interested in learning more about the fascinating phenomena of pathogen interference" if you or another substacker can undertake or share such analysis for a lay audience I, for one, would be very interested to read it x
That is worthy of consideration as a cause for this observed decrease in influenza cases prior to the official presence of COVID.
I had a patient almost die in a local teaching hospital of something that seemed like a viral pneumonia, but moved to his kidneys and circulatory system, almost killing him, in mid November to mid December 2019. The only thing they found was "coronavirus" which was still "just a form of common cold", until a month later.
How much extrapolation was done to get to 17 billion 'flu cases a year? How many were actually colds (man 'flu) and not actually 'flu? US numbers indicate that the pneumonia component of the flu/pneumonia reporting method is a around 95 to 5 pneumonia to flu ratio.
For the C19 dominance of ;flu issue - how much of this is due to false testing using a Drosten RT-PCR test - with 'flu cases being reported as SARS-COV2? Did the testing stop looking for 'flu?
I think the premise that C19 was circulating way before - at least the summer of 2019 - is valid. I wonder if the same testing standards were applied a decade before (over 2009-2018 for example) using the Drosten RT-PCR test, that the virus would have been "detected" then.
Then, again as a lay person, I wonder that if the 2.2 'flu infections is accurate, maybe, just maybe, 'flu is a normal response by the bodies immune system to rid itself of what it doesn't like - in other words, simply discharging excesses accumulated. Totally natural and required for survival of any species.
Lastly, I also wonder if flu prevalence is directly correlated to the levels of "vaccines" - as far as I can make out, the success of 'flu vaccines is a coin toss, based on inoculating against strains guessed to be circulating next years 9and using southern hemisphere as a base - though why the reverse isn't true is beyond me!). The 'flu vaccines may have similar side effects as far as adverse events are concerned and I note that no work is undertaken to correlate the long term effects of contaminants in the flu vaccine and the vaccine itself - with autism, Alzheimer's, ADHD, heart disease and other leading causes of death and disability.
So, that's one lay person's perspective! Which explains why I am just that!
As indicated in the article I share your concerns regarding the Chinese data. I think your thoughts on an immune response such as flu is along the right lines and recognising when people are truly infectious is a difficult task. As a Nobel prize winner stated about my posts;
"Easily read thread by Stephen Andrews.
Good thing about COVID-19 is that Everyone is an Epidemiologist these days. Said despairingly by Neil Ferguson about me (Michael Levitt - Stanford) in Apr 2020 on the BBC It may well improve the world."
I would have loved to have seen this historical data as well as it would added perspective. However a combination of the two studies and other data point us in the pathogen interference direction.
What everyone seems to ignore is the fact that the source of both COVID-19 and the mRNA injection are from the same group  that are trying to build profit and reduce world population. Both contain the same spike protein just in different quantities. As Tennessee Ernie Ford used to sing if the first one don’t get you the second one will.
Boy, I wish I had this available about a year ago when arguing with a med student on the efficacy of masks against viruses. He stated the fact that flu had disappeared during covid was proof masks worked against viruses. Ignoring for the moment that if they worked against the flu so well that it disappeared, why then is covid still spreading, I brought up this condition you describe of one infectious agent suppressing others. The med student said I didn’t know what I was talking about, that no such thing exists.
Not to take away from your excellent research, but it's "toe the line", not "tow the line". It comes from holding a footrace, and "toeing" the starting line. ;-)
I am aware that this expression comes from placing your toe on the starting line but tow seems more evocative.
Stephen the "seasonal signal" that Hope-Simpson was looking for is almost certainly just temperature.
Respiratory viruses need to keep out of our lungs/sinuses etc, in order to keep us moving around. They (almost all) seem to do this by sensing temperature - they are more active below the normal body temperature of their host.
What Hope-Simpson didn't get is that resp viruses adapt to their local climate and season in a few months by gaining or losing thermal sensitivity. They have to lose thermal sensitivity in the Tropics in order to replicate at all. In cold regions nearer the poles they have to gain thermal sensitivity to stop us going to bed very quickly with a fever and not spreading the virus much.
CoV-2 (and influenza etc) is thermally sensitive in the wet-lab and in animals:
https://doi.org/10.1016/j.imj.2022.08.005
Or review: https://doi.org/10.1002/rmv.2241
I do not know whether you have had a chance to look at any of my other substack articles? This one provides experimental evidence on the ability of uv light to facilitate covid-19 cell entry;
https://open.substack.com/pub/sandrews/p/is-this-one-of-the-most-important?utm_source=share&utm_medium=android
I do know Hope-Simpson's work very well. As I mentioned, what he didn't get is that pretty well all respiratory viruses are thermally-sensitive (more active below normal body temp of their host), but they have to adapt their thermal sensitivity to their local climate and season. This takes a few months.
I'm not sure of the details of your hypothesis, but I have several comments
1. Colds and flu don't follow cloudy weather, and are not suppressed by sunny weather. They follow COLD weather. There are many refs for this - see our review - but a good one is Lidwell
Lidwell, O., Morgan, R., & Williams, R. (1965). The epidemiology of the common cold IV. The effect of weather. Journal of Hygiene, 63(3), 427-439. doi:10.1017/S0022172400045319
2. Colds and flu persist at intermediate levels year-round in the Tropics. This is because strains there lose their thermal sensitivity - because they have to. This explains why eg flu tends to go from hot places to colder (see figure 14 in our review)
Our review is here: https://doi.org/10.1002/rmv.2241
3. Most transmission takes place indoors. The amount of time we spend indoors varies by only about 1 hour between summer and winter. (The amount of time we spend outdoors varies a lot, but so what?)
4. In any case I think this argument is settled by the observation that CoV-2 is thermally sensitive in the wet-lab and in animals: https://doi.org/10.1016/j.imj.2022.08.005
We cite 7 papers in our letter, but there are more.
I'll read the papers you cite - I haven't seen them all.
Stephen I don't understand your hypothesis. UV can't get into the nose and throat
This is from one of my Substack articles. Hopefully it expands on the concept. The paper I sent you is just further experimental evidence on the impact of UV light to facilitate cell entry;
The control and regulation of the latent / lysogenic cycles and the movement to the lytic cycles are the key to successful replication of the covid-19 virus. The virus mutates during the lysogenic cycle due to errors in replication. It is proposed that covid-19 initially circulated within a high proportion of the global population at a low level but highly transmissible state and during this phase only mild illness was experienced in the majority of infected individuals. During this infection period a degrees of specific immunity were developed to the prevailing variant(s) in the population. Through a phenomena called quorum sensing (1)(2)(3)(4) the virus has the ability to detect infected host cell availability through chemical signals that have the capability to regulate the lytic infection cycle. A second mechanism of cycle regulation involves highly specific conditions of ultraviolet (UV) light that exist at different times of the day and seasonally. The virus is being continually exhaled by infected individuals at a low level and the viral particles are being modified by the specific conditions of UV light. The modification could involve specific cleavage of the virus into smaller fragments. A proportion of these viral fragments are inhaled by the host, due to the proximity to their own breath. The concentration of these fragments have the capability to act as a feedback signal that a successful variant has escaped the immune system and also conditions are more favourable for external existence and therefore transmission. The movement from the lysogenic to the lytic cycle will be accelerated on the basis of the concentration and specificity of these fragments. The product of both of these continuous feedback cycles reach a threshold level and the selected mutated state of the virus moves to an intense lytic phase releasing favourable mutations and infecting further individuals with potentially more vulnerable immune systems. The seasonally /UV activated period of high infectivity is relatively brief as the reactivated individuals immune system responds to the “high level” lytic cycle challenge. Those individuals exposed to the “new” mutation(s) who mount a more severe immune response do not have a sufficient “new” viral load to be significantly infectious. The release of the selected mutation results in a more serious impact on less healthy immune systems with particular emphasis on the aged through immunosenescence. The overall goal of these two feedback mechanisms is to facilitate successful replication of the virus in the ongoing battle with the host’s immune systems. The emergence of successful variants such as Alpha, Delta and Omicron are a product of this selection process. A high proportion of individuals have immunity from prior coronovirus infections and, depending on the prevalent mutation, not susceptible to infection from that specific mutation. They may be carrying the virus in a latent / lysogenic mutating form but their immune system will resist viral escape and therefore will be receiving a limited feedback chemical signal to increase replication or move to an intense lytic cycle.
Thanks for engaging in a dialogue which has been sadly missing during this whole covid-19 debacle.
Thanks for your reply!
The most obvious difference between summer and winter is that it is colder in winter.
Is there any reason why you think that these cycles are not driven by temperature, as suggested by the wet-lab and animal studies that we cited?
I'm not clear how UV comes into the picture. I think the study you sent is about exposing cells to UV - isn't it?
It is pretty simple really. UV light is high energy. It will be correlated with temperature. It is almost a perfect fit for Hope-Simpson's proposition's. I have never had anyone challenge this thinking.
Does "pathogenic interference" counter allegations that the March 2020 changes in disease reporting protocols allowed central planners to "muscle out" other seasonal respiratory illnesses and propel the novel virus, lockdown narrative?
Without commenting on your analysis, which seems excellent, I want to make another point. This point seems more and more unassailable to me, as the days since the advent of the Great Covid Dumpster Fire go by. How the absolute freaking hell did the B.S. that is mistaken for public health succeed for so long, when there are people like you and so many others, including Joel, out here to show the folly? I realize the scam runs deep, but seriously, Dr. Fauci is a moron compared to many folks writing on Substack. Are we, as a species, that stupid? (Don't answer that!)
"The chemical signalling that exists between viruses, hosts and bacteria have been known for very many years (7). This was ignored during the pandemic. If you are interested in learning more about the fascinating phenomena of pathogen interference" if you or another substacker can undertake or share such analysis for a lay audience I, for one, would be very interested to read it x
Hopefully the references that I cited on the bottom of the article should link to the correct reference?
Thank you for your excellent post.
Great article, but:
s/to tow the line/to toe the line/
You put your toes on the line to line up in a row in the military.
The Ethical Skeptic makes a very well substantiated case that SARS-Cov2 could well have been circulating since early 2018. https://theethicalskeptic.com/2021/11/15/chinas-ccp-concealed-sars-cov-2-presence-in-china-as-far-back-as-march-2018/
That is worthy of consideration as a cause for this observed decrease in influenza cases prior to the official presence of COVID.
I had a patient almost die in a local teaching hospital of something that seemed like a viral pneumonia, but moved to his kidneys and circulatory system, almost killing him, in mid November to mid December 2019. The only thing they found was "coronavirus" which was still "just a form of common cold", until a month later.
Interesting!
As a lay person, my first reactions were:
How much extrapolation was done to get to 17 billion 'flu cases a year? How many were actually colds (man 'flu) and not actually 'flu? US numbers indicate that the pneumonia component of the flu/pneumonia reporting method is a around 95 to 5 pneumonia to flu ratio.
For the C19 dominance of ;flu issue - how much of this is due to false testing using a Drosten RT-PCR test - with 'flu cases being reported as SARS-COV2? Did the testing stop looking for 'flu?
I think the premise that C19 was circulating way before - at least the summer of 2019 - is valid. I wonder if the same testing standards were applied a decade before (over 2009-2018 for example) using the Drosten RT-PCR test, that the virus would have been "detected" then.
I wonder how many reports of work in the Ukraine bio-labs has been "black noticed" and suppressed. See here: https://www.europarl.europa.eu/doceo/document/P-8-2016-000636_EN.html?redirect
Then, again as a lay person, I wonder that if the 2.2 'flu infections is accurate, maybe, just maybe, 'flu is a normal response by the bodies immune system to rid itself of what it doesn't like - in other words, simply discharging excesses accumulated. Totally natural and required for survival of any species.
Lastly, I also wonder if flu prevalence is directly correlated to the levels of "vaccines" - as far as I can make out, the success of 'flu vaccines is a coin toss, based on inoculating against strains guessed to be circulating next years 9and using southern hemisphere as a base - though why the reverse isn't true is beyond me!). The 'flu vaccines may have similar side effects as far as adverse events are concerned and I note that no work is undertaken to correlate the long term effects of contaminants in the flu vaccine and the vaccine itself - with autism, Alzheimer's, ADHD, heart disease and other leading causes of death and disability.
So, that's one lay person's perspective! Which explains why I am just that!
As indicated in the article I share your concerns regarding the Chinese data. I think your thoughts on an immune response such as flu is along the right lines and recognising when people are truly infectious is a difficult task. As a Nobel prize winner stated about my posts;
"Easily read thread by Stephen Andrews.
Good thing about COVID-19 is that Everyone is an Epidemiologist these days. Said despairingly by Neil Ferguson about me (Michael Levitt - Stanford) in Apr 2020 on the BBC It may well improve the world."
Even to a layman things should make sense!!
even at best the "flu vaccine" has only been shown to be 8% effective, ie zero if you count natural immunity
What does such a streamgraph look like for earlier time periods? What is the Y axis?
(ie: what are the seasonal patterns for normal years)
I would have loved to have seen this historical data as well as it would added perspective. However a combination of the two studies and other data point us in the pathogen interference direction.