On a kind of related topic, I came across these two papers recently which essentially explain why the modRNA vaccines cannot prevent the spread of the SARS-CoV-2 virus (note, I am not saying anything about whether they affect severity of the disease.)
Rethinking next-generation vaccines for coronaviruses, influenzaviruses, and other respiratory viruses
"In this review, we examine challenges that have impeded development of effective mucosal respiratory vaccines, emphasizing that all of these viruses replicate extremely rapidly in the surface epithelium and are quickly transmitted to other hosts, within a narrow window of time before adaptive immune responses are fully marshaled."
SARS-CoV-2 replication in airway epithelia requires motile cilia and microvillar reprogramming
Imo, since they temporarily prevent infection in the first place, they also stop spread. Then you have to go back to early 2021, were they going to prevent infection long term, nobody actually knew because that was in the future. Everyone should have been able to tell this for themselves though. If a car company tells you they just designed and built your new car last month, then promises you it will last x time / miles, it's on you if you believe something they can't possibly know yet.
Assuming "they" here are the vaccines, the issue seems to me to be that they are injectable vaccines and those do not seem to prevent infection of the nasal epithelial cells and transmission. As the authors of paper 2 say:
"Nasal and upper airway CECs are the main targets for initial COVID-19 infections.2,10,11,12,13 Many respiratory viruses, including SARS-CoV-1,14 influenza,15 parainfluenza (PIV),16 rhinovirus (RV),17,18 and respiratory syncytial virus (RSV),19 first infect airway CECs. SARS-CoV-2 receptors ACE2 and TMPRSS2 localize to cilia in CECs.20,21 Here, we report that SARS-CoV-2 infects nasal mucosa by a two-step process. First, SARS-CoV-2 particles bind the ACE2 receptor on the surface of airway cilia. Cilia then facilitate virus transport through the PCL mucin layer. Initially, only a few ciliated human nasal epithelial cells (HNEs) are productively infected. Within the next 24 h SARS-CoV-2 hijacks the host cell machinery to induce elongated and highly branched microvilli. This rearrangement requires protein kinases, including p21-activated kinases 1 and 4 (PAK1/4). Activating p21-activated kinases (PAK) enables the virus to exit across the PCL layer before lateral spread to other regions, potentially via mucociliary transport (MCT)."
Injection isn't prima facie relevant. The immune system is a collection of specific responses and they aren't categorically separated like Army vs. police or some such thing.
If the problem is that the virus infects the nose, does this mean it's just unstoppable, or? The issue at hand is how is it stopped (if it is), the specific things that the immune system does, again these aren't categorically separated. If you have antibodies in the blood, they can elute to the mucosa. Is this enough? Yes? No? So if you observe that people aren't getting sick and aren't testing positive for a few months after vaccination, and the idea is this is impossible, either you are saying the antibodies don't wind up in the mucosa or they don't work there somehow. The former is false, it has been measured, both IgG and IgA appear after vaccination, less than in blood but still there. The latter is just a theory without any basis, and doesn't match the evidence (no reported infections for a few months).
I had never heard of diphtheria until moving to the US, but then I lived in fairly spread out areas in Australia for my first 19 years. That is none of them had large populations. Also, there seemed to be no knowledge about it.
However, I just asked a person from Hong Kong if they had heard of it (or the Chinese name for it) and she had not. Also, a quick search revealed no info on the history of diphtheria in China, which is strange because they have had very large cities for quite a while and HK has been a large city for quite some time. Maybe opium was a bigger problem for them.
Large cities, but in a large area - so they end up being insulated from each other. Industrial Era European urbanization puts large, crowded settlements in close proximity so even if a toxigenic strain burns out in one city the others re-seed it.
Trying to reconcile this account of diphtheria with, say, Laura Ingalls Wilder's account of it, where her whole family came down with it in their rural home in DeSmet ND in 1888. Surely that wasn't on account of urbanization? Since the contagion seemed to be both from "walking" cases as well as sewage... would speedier transport (i.e. railroads) have extended the reach of the disease into rural communities connected by train? I wonder if there's any way to compare communities with regular train service, to communities that were a good distance from the nearest railway?
The model posits massively increased rural incidence after 1885.
Rural areas always existed. They didn't have to worry about urban centers being incubators for pathogens until urban centers existed on a large scale. Once this happened, rural diphtheria no longer operated under the selection penalties that kept toxigenic strains dying out before, because even if they died out in rural areas they were just re-imported from urban centers over and over.
The details of this second paradox -- rural sometimes more badly affected -- will be hashed in a follow-up post. As for rail, certainly must have helped to spread, but attributing rural diphtheria to it is also redundant. The rail still has to take the diphtheria from the cities. The cities didn't exist before 1830. Diphtheria isn't in the cities before 1855-1880, but once it is, it's also in rural areas. Sweden, which gives us good numbers, isn't as urbanized as others, but since all of Europe rapidly becomes "infested" after the UK it doesn't make a big difference, lots of diphtheria. Same with Serbia, very backward nation though there was rail investment from AH Empire, super-high rates of diphtheria. So even without rail it gets to rural areas.
Lots of city electric wires installed in the cities around that time would be my guess. Pictures I have seen of the wires look ridiculous in density and very low to the ground.
Rates soon become higher in rural areas. This is spillover from the cities. So the explanation should remain confined to the host and pathogen otherwise it makes no sense for the problem to escape from cities to rural
On a kind of related topic, I came across these two papers recently which essentially explain why the modRNA vaccines cannot prevent the spread of the SARS-CoV-2 virus (note, I am not saying anything about whether they affect severity of the disease.)
Rethinking next-generation vaccines for coronaviruses, influenzaviruses, and other respiratory viruses
https://www.cell.com/cell-host-microbe/fulltext/S1931-3128(22)00572-8
Authors include Fauci and it is from 2022/2023.
"In this review, we examine challenges that have impeded development of effective mucosal respiratory vaccines, emphasizing that all of these viruses replicate extremely rapidly in the surface epithelium and are quickly transmitted to other hosts, within a narrow window of time before adaptive immune responses are fully marshaled."
SARS-CoV-2 replication in airway epithelia requires motile cilia and microvillar reprogramming
https://www.cell.com/cell/fulltext/S0092-8674(22)01505-7
Published a little before the one above. Authors from Standford.
This article provides exquisite descriptions of the mechanisms of entry and exit for various respiratory viruses and seems above reproach.
PAK1 blockers would seem to be useful, and D3 and IVM are PAK1 blockers but you can search for articles on those.
Imo, since they temporarily prevent infection in the first place, they also stop spread. Then you have to go back to early 2021, were they going to prevent infection long term, nobody actually knew because that was in the future. Everyone should have been able to tell this for themselves though. If a car company tells you they just designed and built your new car last month, then promises you it will last x time / miles, it's on you if you believe something they can't possibly know yet.
Assuming "they" here are the vaccines, the issue seems to me to be that they are injectable vaccines and those do not seem to prevent infection of the nasal epithelial cells and transmission. As the authors of paper 2 say:
"Nasal and upper airway CECs are the main targets for initial COVID-19 infections.2,10,11,12,13 Many respiratory viruses, including SARS-CoV-1,14 influenza,15 parainfluenza (PIV),16 rhinovirus (RV),17,18 and respiratory syncytial virus (RSV),19 first infect airway CECs. SARS-CoV-2 receptors ACE2 and TMPRSS2 localize to cilia in CECs.20,21 Here, we report that SARS-CoV-2 infects nasal mucosa by a two-step process. First, SARS-CoV-2 particles bind the ACE2 receptor on the surface of airway cilia. Cilia then facilitate virus transport through the PCL mucin layer. Initially, only a few ciliated human nasal epithelial cells (HNEs) are productively infected. Within the next 24 h SARS-CoV-2 hijacks the host cell machinery to induce elongated and highly branched microvilli. This rearrangement requires protein kinases, including p21-activated kinases 1 and 4 (PAK1/4). Activating p21-activated kinases (PAK) enables the virus to exit across the PCL layer before lateral spread to other regions, potentially via mucociliary transport (MCT)."
Injection isn't prima facie relevant. The immune system is a collection of specific responses and they aren't categorically separated like Army vs. police or some such thing.
If the problem is that the virus infects the nose, does this mean it's just unstoppable, or? The issue at hand is how is it stopped (if it is), the specific things that the immune system does, again these aren't categorically separated. If you have antibodies in the blood, they can elute to the mucosa. Is this enough? Yes? No? So if you observe that people aren't getting sick and aren't testing positive for a few months after vaccination, and the idea is this is impossible, either you are saying the antibodies don't wind up in the mucosa or they don't work there somehow. The former is false, it has been measured, both IgG and IgA appear after vaccination, less than in blood but still there. The latter is just a theory without any basis, and doesn't match the evidence (no reported infections for a few months).
There are claims in various places that Diphtheria toxicity is a result of infection by a phage.
If that is true, it adds an extra wrinkle to the story.
I had never heard of diphtheria until moving to the US, but then I lived in fairly spread out areas in Australia for my first 19 years. That is none of them had large populations. Also, there seemed to be no knowledge about it.
However, I just asked a person from Hong Kong if they had heard of it (or the Chinese name for it) and she had not. Also, a quick search revealed no info on the history of diphtheria in China, which is strange because they have had very large cities for quite a while and HK has been a large city for quite some time. Maybe opium was a bigger problem for them.
Large cities, but in a large area - so they end up being insulated from each other. Industrial Era European urbanization puts large, crowded settlements in close proximity so even if a toxigenic strain burns out in one city the others re-seed it.
Trying to reconcile this account of diphtheria with, say, Laura Ingalls Wilder's account of it, where her whole family came down with it in their rural home in DeSmet ND in 1888. Surely that wasn't on account of urbanization? Since the contagion seemed to be both from "walking" cases as well as sewage... would speedier transport (i.e. railroads) have extended the reach of the disease into rural communities connected by train? I wonder if there's any way to compare communities with regular train service, to communities that were a good distance from the nearest railway?
The model posits massively increased rural incidence after 1885.
Rural areas always existed. They didn't have to worry about urban centers being incubators for pathogens until urban centers existed on a large scale. Once this happened, rural diphtheria no longer operated under the selection penalties that kept toxigenic strains dying out before, because even if they died out in rural areas they were just re-imported from urban centers over and over.
The details of this second paradox -- rural sometimes more badly affected -- will be hashed in a follow-up post. As for rail, certainly must have helped to spread, but attributing rural diphtheria to it is also redundant. The rail still has to take the diphtheria from the cities. The cities didn't exist before 1830. Diphtheria isn't in the cities before 1855-1880, but once it is, it's also in rural areas. Sweden, which gives us good numbers, isn't as urbanized as others, but since all of Europe rapidly becomes "infested" after the UK it doesn't make a big difference, lots of diphtheria. Same with Serbia, very backward nation though there was rail investment from AH Empire, super-high rates of diphtheria. So even without rail it gets to rural areas.
Lots of city electric wires installed in the cities around that time would be my guess. Pictures I have seen of the wires look ridiculous in density and very low to the ground.
Rates soon become higher in rural areas. This is spillover from the cities. So the explanation should remain confined to the host and pathogen otherwise it makes no sense for the problem to escape from cities to rural