J’ACCUSE! THE SPIKE ANTIBODY/FC-RECEPTOR COMPLEX IS SOURCE OF SEVERE COVID AND THE INDUCTION OF SYSTEMIC AUTOIMMUNE DISEASE: ONE SIDE OF THE AUTOIMMUNE/AMYLOIDOSIS SARS-CoV-2 COIN - AND IT WAS KNOWN!
J’ACCUSE! THE SPIKE ANTIBODY/FC-RECEPTOR COMPLEX IS SOURCE OF SEVERE COVID AND THE INDUCTION OF SYSTEMIC AUTOIMMUNE DISEASE: ONE SIDE OF THE AUTOIMMUNE/AMYLOIDOSIS SARS-CoV-2 COIN - AND IT WAS KNOWN!
Jul 7, 2022·edited Jul 7, 2022Liked by Walter M Chesnut
Bingo Walter! I’ve been waiting for this. I measure SARS-CoV-2 Semi Quant. Total Spike antibodies in all my patients, if possible, and there appears to be a strong correlation between severity of symptoms and disease presentation and level of antibodies.
One of my patients never vaccinated receiving monthly IVIG infusions since at least early 2021 all of a sudden after her December treatment showed very elevated levels of Spike antibodies, in the many thousands where as she did not have higher than 100 previously after community acquired infection. Therefore I suspect that the IVIG supply is contaminated.
A family member is on IvIG for (ironically) a flu/MMR vaccine induced autoimmune disorder. Their antibody levels have shown as ZERO/uninfected on 2 occasions, which is odd as per an early 2021 study, 66-ish% of all IvIG supplies tested positive for covid antibodies from Sept 2020 (from recollection).
Anyway... I've been long concerned about a tainted IvIG supply, but it seems they've dodged the bullet thus far due to the ZERO antibody tests, but ti seems I should still be worried.
Mexico will pay for the wall-To keep the U.S. out (also-they are the richest country in silver in the world, which has been stolen from the citizens for decades/centuries).
I can help you a bit on this one. I haven't put the diagrams in articles, but have presented them during interviews---the DMED data shows a clear increase in severity of COVID-19 infections among the military (similar age/health profiles with little chance for Simpson's paradoxes). I will put this together in an article and link back here.
It seems to me you are saying something very important and simple. A lot depends on the neutrophil/lymphocyte ratio. In young people there is an aggressive innate response with NK cells, but as we get older the ratio turns towards greater dependence on leukocytes, causing inflammation and the neutrophils get activated because of ADE and release an enzyme that starts the amyloidosis process whilst also igniting the NLRP3 inflammasome. This combo is the essence of the pathology of SARS-2. Check your CRP and NLR blood work and take Zinc/ Quercetin /ivermectin for the virus, niacin for inflammation, and Tumeric/Lumbrokinase to dissolve amyloid and Olive leaf for all the above.
Jul 7, 2022·edited Jul 7, 2022Liked by Walter M Chesnut
I saw that Shi Zhengli ADE paper very early on. Like, the same month it was published. It was one of the first things that convinced me to dig deeper. Very concerning.
On the one hand we have many saying don't live in fear and go about your life and on the other hand we have Walter saying data says to limit exposures. I don't want to live in fear of exposures. We are all unvaxxed, had mild covid in Dec 2021, have good vitamin d levels and use high doses of vitamin c, probiotics and quercitin/zinc. It is difficult to know what to do. I certainly don't want more lockdowns/masks which people will want if Walter is indeed correct. Living under a rock in fear of dying is no life. I just don't believe there aren't natural ways to mitigate the harm of the spike.
I appears that they are saying if you have no co-morbidities, no immune-senescence or elderly and not vaccinated, you are fine. Quercetin and Tumeric stop amyloidosis and Zinc blocks viral import like ivermectin.
I'm with you. However, it looks like these two key sentences from the two papers will help us figure it out:
1. "This may, at long last, explain why there seems to be more severe disease at points post vaccination and why, if the virus is not cleared, the DOSAGE of antibodies within the body from infection can then cause progression of the disease!"
2. "Could it be that those who “lose” antibodies more quickly post-infection, ironically, fare better in the long run?"
So they are basically saying - Usually, the more antibodies, the better. Not so here. The antibodies will trigger autoimmune disease. The people who can get rid of these antibodies quickly, will actually do better. So now they are trying to figure out ways to therapeutically reduce the number of antibodies. That's the question. How to reduce the number of antibodies. That's what cc is suggesting above with colostrum with the high immuglobulin question.
Thank you SAMO. I now get it. So then, getting boosters of the original Wuhan virus is a bad idea indeed. Not only will it prolong infections circulating within communities; it will needlessly raise antibody levels again, to the detriment of the boosted! (Not to mention possible adverse events also. . . )
that's the community here for with plenty of smart and kind people .... let Walter do his own thing as more comfortable to him, cant bother him to translate it to us.
Pretend you have 100 white blood cells. Each attaches to a specific antibody and goes hunting. If 40 of those white blood cells attach to the "bad" antibody, then chaos ensues.
IVIG pumps in a bunch of other antibodies for the white blood cells to attach to. So, rather than 40 WBC getting the "bad" antibody. only 10 do.
The medical thought is that IVIG reduces your immune system/response because it waters it down across a bunch of antibodies. However, that's kinda like saying you're dumber because you have a library of books rather than a bookcase. Sure, overloading the immune system at the wrong time could keep too many of those 100 WBCs from attaching to "good" antibodies, but generally... I think a larger library of antibodies are a good thing.
Jul 7, 2022·edited Jul 8, 2022Liked by Walter M Chesnut
Yeah, very technical. I'm trying to understand the basics. This is as far as I got:
-Antibodies stick to the virus so the virus doesn't enter/infect our healthy cells.
-antibody dependent enhancement (ADE) occurs when antibodies help the virus enter our cells, rather than prevent it.
-in ADE, if there are a large number of antibodies stuck to viruses, there will be way more viruses entering healthy cells and causing more disease. Fewer antibodies means fewer viruses entering healthy cells causing less disease.
-Fc receptors are on the surface of leukocytes (white blood cells that are part of the immune system).
-Fc receptors bind to antibodies that are stuck to the virus.
-there are different types of Fc receptors on the white blood cells. FcγRIIB is the only inhibitory Fc receptor. It controls many aspects of immune and inflammatory responses.
-the antibodies that are attached to the virus happen to bind to FcγRIIB on the white blood cells, and I assume this blocks it's inhibitory function, causing more autoimmune disease.
-more antibodies that bind to FcγRIIB equates to more autoimmune disease. Less antibodies binding, less autoimmune disease.
Walter, every single of your posts is more amazing than even the last. I can almost hear the whistling sound of a bomb dropping every time I see your name in my feed. You are still so very missed on the twitter (as is now Jikky 🐭 x 2, sadly). I have been wondering if you think there is any utility in autophagy’s ability to clear spike or prevent the kinda of outcomes you theorize? I wonder because of a few things you and Jessica have each said over these many months and because I read a long while back a reference to the jabs lowering recipients’ ability to enter autophagy; tho I can’t say where it stuck hard with me (also considering how in the US so many are affected by metabolic dysfunction/obesity and how obesity is considered something of a dire comorbidity with the virus).
ICU cases of Covid-19 are caused by two lethal antibodies: REGN10987 and B38. That is why Uracil was replaced with Pseudouridine, in order to sabotage the immune system in producing isomeric (binding) antibodies. Since Uracil has been substituted with Pseudouridine, this means that the vaccines are cmRNA and not mRNA: had the vaccines been mRNA, all of the vaccinees would have found themselves in ICU with severe cases of Covid-19 because of the two lethal antibodies listed above. The huge problem now is constituted by the ISOMERIC ABS.
Spike proteins = dextrorotatory prions = T-bacilli. D-prions (beta sheet prions) absorb the oxygen and cause hypoxia and micro blood clots. Spike proteins coded with Pseudouridine are even more prone to reach a dextrorotatory state (chirality).
Omicron is Mers-Cov-2 since it uses the DPP4 celullar receptor. There are no viruses only mycobacterium and mycoplasma. Sars-Cov-2 is actually M. avium accompanied by passenger mycoplasma such as Chlamydia pneumoniae. Omicron is M. influenzae (aka Mers-Cov, aka H1N1).
1915-1917 worldwide pandemic of "coronavirus", actually M. avium
1918 M. influenzae which in the course of a single day became M. africanum (galloping tuberculosis)
2019-2021 M. avium (Sars-Cov-2)
2022 M. influenzae/Omicron (Mers-Cov-2)
The difference between Omicron and Delta is that Omicron has not had, yet, its prion domain activated.
MPV is still Sars-Cov-2 (poxviridae is a mycobacterium, a variant of M. leprae), Sars-Cov-2 has some 20 sequences of amino acids from the most lethal pathogens known today (M. tuberculosis, B. anthracis, Y. pestis, M. bovis, M. leprae).
Im happy that I found you so now I know Im not alone. I was just suspicious about all this but could not to find all the info needed to stick the mycoplasma hypothesis together. Thank you, Sandokhan!
At the time (february-april 2003), the official line in China was that atypical pneumonia (SARS), as it was then called, was caused by a Chlamydia bacterium, says Yang Ruifu, a soft-spoken microbiologist and a member of the team at the Academy of Military Medical Sciences (AMMS) that discovered the coronavirus.
In some few sections, coronavirus-like particles were concurrently seen. A coronavirus RNA- polymerase segment (440 bp) was amplified from the lung tissues of two cases of the SARS. After inoculated with materials from the lung samples, the similar Chlamydia-like particles were also found in the inoculated 293 cells. Since the Chlamydia-like agents visualized in both organs and cell cultures could not react with the genus specific antibodies against Chlamydia and monoclonal antibodies against C. pneumoniae and C. psittaci, the results might well be suggestive of a novel Chlamydia-like agent. Since the novel Chlamydia-like agent was found co-existing with a coronavirus-like agent in the dead cases of SARS, it looks most likely that both the agents play some roles in the disease.
Before Covid there was an outbreak of MP Pneumoniae in one of Chinas military unit. I was researching/collecting all I could find about mycoplasma before Covid era. I got interested in it as soon as I read about-common mycoplasma now weaponised. Thanks for links, going to check all of them.
That's disturbing. Definitely up there on the WTF scale. Table 6 in the Shi paper is not particularly comforting. Where bad is varies by tissue type and receptor type. If it happened in mers would it happen in cov2? Well that would explain some things people have been arguing about for a good part of 2021. The whole don't count the vaxed as vaxed because lots of covid in the first 2 weeks after jab then a period of likely protection (very high end antibodies) then a decline and greater susceptibility vs unvaxed. I believe that is the arch Walter is talking about. The statisticians have been saying there is ADE on the back end for a while. Looks like they are right. The avoiding of counting people as vaccinated for 14 days post jab would be an admission that people are more vulnerable during that period as well as a way to pad the numbers on effacacy so it is undoubtably worse that presented. Table 6 seems to indicate a ramp enhancement time for MERS in all but lung DPP4 but one has to wonder about the profile for tissues not tested. Makes me wonder what the covid viral and vax antibody ramp looks like for that 14 day period. Also some of the statisticians were showing negative values against control (unvaxed) meaning vax enhanced disease after a few months using the hospital/ death and cases data. If there were a paper or two profiling antibody levels by month of recovered viral and vaxed one could swag a zone where such things may well be happening based on first 2-3 weeks and maybe about 4 months to 6 months (where the booster was then recommended) on the fist 2 jabs. The signal is strong in the vax profiles which then could be compared to the viral recovered unvaxed to see if there is a problem too. However as far as I am concerned it is enough to know there is a problem overall and to think about how to manage it for prevention, if ill and post exposure of any sort.
Bingo Walter! I’ve been waiting for this. I measure SARS-CoV-2 Semi Quant. Total Spike antibodies in all my patients, if possible, and there appears to be a strong correlation between severity of symptoms and disease presentation and level of antibodies.
One of my patients never vaccinated receiving monthly IVIG infusions since at least early 2021 all of a sudden after her December treatment showed very elevated levels of Spike antibodies, in the many thousands where as she did not have higher than 100 previously after community acquired infection. Therefore I suspect that the IVIG supply is contaminated.
Thank you so much!!
And that confirms what I suspected. That the IvIG supply is, and will forever be, tainted. It is most likely unusable at this point.
Stay away from needles or anything that can be injected into the blood stream.
Have long wondered about contamination: IVIG as well as blood and organ supply.
A family member is on IvIG for (ironically) a flu/MMR vaccine induced autoimmune disorder. Their antibody levels have shown as ZERO/uninfected on 2 occasions, which is odd as per an early 2021 study, 66-ish% of all IvIG supplies tested positive for covid antibodies from Sept 2020 (from recollection).
Anyway... I've been long concerned about a tainted IvIG supply, but it seems they've dodged the bullet thus far due to the ZERO antibody tests, but ti seems I should still be worried.
Mexico will pay for the wall-To keep the U.S. out (also-they are the richest country in silver in the world, which has been stolen from the citizens for decades/centuries).
Me too! A family member is on IvIG so I've had my ear to the ground for the same info. Anything to share would be appreciated!
You will need a quantitative test. None of these seem to include that.
What biomarkers/diagnostics are you using for spike count?
https://www.labcorp.com/tests/164090/sars-cov-2-semi-quantitative-total-antibody-spike
Nice finds!
I can help you a bit on this one. I haven't put the diagrams in articles, but have presented them during interviews---the DMED data shows a clear increase in severity of COVID-19 infections among the military (similar age/health profiles with little chance for Simpson's paradoxes). I will put this together in an article and link back here.
Cheers.
Link?
I wonder if Colostrum with high immuglobulin would be helpful for those who could not get the intravenous treatment?
ADE was always bound to happen due to the repeated use of non sterilising etc “vaccines” Thanks for this excellent article, I will share this.
It seems to me you are saying something very important and simple. A lot depends on the neutrophil/lymphocyte ratio. In young people there is an aggressive innate response with NK cells, but as we get older the ratio turns towards greater dependence on leukocytes, causing inflammation and the neutrophils get activated because of ADE and release an enzyme that starts the amyloidosis process whilst also igniting the NLRP3 inflammasome. This combo is the essence of the pathology of SARS-2. Check your CRP and NLR blood work and take Zinc/ Quercetin /ivermectin for the virus, niacin for inflammation, and Tumeric/Lumbrokinase to dissolve amyloid and Olive leaf for all the above.
I saw that Shi Zhengli ADE paper very early on. Like, the same month it was published. It was one of the first things that convinced me to dig deeper. Very concerning.
Thanks, Walter.
I will share it to about 20 Aussie "experts", including CHOs - they are my unrequited penpals.
On the one hand we have many saying don't live in fear and go about your life and on the other hand we have Walter saying data says to limit exposures. I don't want to live in fear of exposures. We are all unvaxxed, had mild covid in Dec 2021, have good vitamin d levels and use high doses of vitamin c, probiotics and quercitin/zinc. It is difficult to know what to do. I certainly don't want more lockdowns/masks which people will want if Walter is indeed correct. Living under a rock in fear of dying is no life. I just don't believe there aren't natural ways to mitigate the harm of the spike.
I appears that they are saying if you have no co-morbidities, no immune-senescence or elderly and not vaccinated, you are fine. Quercetin and Tumeric stop amyloidosis and Zinc blocks viral import like ivermectin.
thank you to both you and walter !!!
it is not about living in fear, it is about being careful ... as he said. i am sending you as sheep among wolves ...
Excellent, always!!!
Would someone please describe the main gist of this post in laymen terms? This will take me a while to understand. . . a bit too technical for me.
I'm with you. However, it looks like these two key sentences from the two papers will help us figure it out:
1. "This may, at long last, explain why there seems to be more severe disease at points post vaccination and why, if the virus is not cleared, the DOSAGE of antibodies within the body from infection can then cause progression of the disease!"
2. "Could it be that those who “lose” antibodies more quickly post-infection, ironically, fare better in the long run?"
So they are basically saying - Usually, the more antibodies, the better. Not so here. The antibodies will trigger autoimmune disease. The people who can get rid of these antibodies quickly, will actually do better. So now they are trying to figure out ways to therapeutically reduce the number of antibodies. That's the question. How to reduce the number of antibodies. That's what cc is suggesting above with colostrum with the high immuglobulin question.
Thank you SAMO. I now get it. So then, getting boosters of the original Wuhan virus is a bad idea indeed. Not only will it prolong infections circulating within communities; it will needlessly raise antibody levels again, to the detriment of the boosted! (Not to mention possible adverse events also. . . )
interesting ... makes total sense
This makes me feel better about my recent lab work showing no antibodies despite having Covid in January (omicron most likely).
that's the community here for with plenty of smart and kind people .... let Walter do his own thing as more comfortable to him, cant bother him to translate it to us.
Pretend you have 100 white blood cells. Each attaches to a specific antibody and goes hunting. If 40 of those white blood cells attach to the "bad" antibody, then chaos ensues.
IVIG pumps in a bunch of other antibodies for the white blood cells to attach to. So, rather than 40 WBC getting the "bad" antibody. only 10 do.
The medical thought is that IVIG reduces your immune system/response because it waters it down across a bunch of antibodies. However, that's kinda like saying you're dumber because you have a library of books rather than a bookcase. Sure, overloading the immune system at the wrong time could keep too many of those 100 WBCs from attaching to "good" antibodies, but generally... I think a larger library of antibodies are a good thing.
Yeah, very technical. I'm trying to understand the basics. This is as far as I got:
-Antibodies stick to the virus so the virus doesn't enter/infect our healthy cells.
-antibody dependent enhancement (ADE) occurs when antibodies help the virus enter our cells, rather than prevent it.
-in ADE, if there are a large number of antibodies stuck to viruses, there will be way more viruses entering healthy cells and causing more disease. Fewer antibodies means fewer viruses entering healthy cells causing less disease.
-Fc receptors are on the surface of leukocytes (white blood cells that are part of the immune system).
-Fc receptors bind to antibodies that are stuck to the virus.
-there are different types of Fc receptors on the white blood cells. FcγRIIB is the only inhibitory Fc receptor. It controls many aspects of immune and inflammatory responses.
-the antibodies that are attached to the virus happen to bind to FcγRIIB on the white blood cells, and I assume this blocks it's inhibitory function, causing more autoimmune disease.
-more antibodies that bind to FcγRIIB equates to more autoimmune disease. Less antibodies binding, less autoimmune disease.
Thank you!
Love the French reference of the Dreyfus Affair Walter.
Saving and sharing. Thank you Walter.
What are the implications for someone who received monoclonal antibodies (satrovimab) back in January this year.
Walter, every single of your posts is more amazing than even the last. I can almost hear the whistling sound of a bomb dropping every time I see your name in my feed. You are still so very missed on the twitter (as is now Jikky 🐭 x 2, sadly). I have been wondering if you think there is any utility in autophagy’s ability to clear spike or prevent the kinda of outcomes you theorize? I wonder because of a few things you and Jessica have each said over these many months and because I read a long while back a reference to the jabs lowering recipients’ ability to enter autophagy; tho I can’t say where it stuck hard with me (also considering how in the US so many are affected by metabolic dysfunction/obesity and how obesity is considered something of a dire comorbidity with the virus).
Saw this this morning. https://nutrition.bmj.com/content/early/2022/06/30/bmjnph-2022-000462
ICU cases of Covid-19 are caused by two lethal antibodies: REGN10987 and B38. That is why Uracil was replaced with Pseudouridine, in order to sabotage the immune system in producing isomeric (binding) antibodies. Since Uracil has been substituted with Pseudouridine, this means that the vaccines are cmRNA and not mRNA: had the vaccines been mRNA, all of the vaccinees would have found themselves in ICU with severe cases of Covid-19 because of the two lethal antibodies listed above. The huge problem now is constituted by the ISOMERIC ABS.
Spike proteins = dextrorotatory prions = T-bacilli. D-prions (beta sheet prions) absorb the oxygen and cause hypoxia and micro blood clots. Spike proteins coded with Pseudouridine are even more prone to reach a dextrorotatory state (chirality).
Omicron is Mers-Cov-2 since it uses the DPP4 celullar receptor. There are no viruses only mycobacterium and mycoplasma. Sars-Cov-2 is actually M. avium accompanied by passenger mycoplasma such as Chlamydia pneumoniae. Omicron is M. influenzae (aka Mers-Cov, aka H1N1).
1915-1917 worldwide pandemic of "coronavirus", actually M. avium
1918 M. influenzae which in the course of a single day became M. africanum (galloping tuberculosis)
2019-2021 M. avium (Sars-Cov-2)
2022 M. influenzae/Omicron (Mers-Cov-2)
The difference between Omicron and Delta is that Omicron has not had, yet, its prion domain activated.
MPV is still Sars-Cov-2 (poxviridae is a mycobacterium, a variant of M. leprae), Sars-Cov-2 has some 20 sequences of amino acids from the most lethal pathogens known today (M. tuberculosis, B. anthracis, Y. pestis, M. bovis, M. leprae).
Im happy that I found you so now I know Im not alone. I was just suspicious about all this but could not to find all the info needed to stick the mycoplasma hypothesis together. Thank you, Sandokhan!
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1550436/
At the time (february-april 2003), the official line in China was that atypical pneumonia (SARS), as it was then called, was caused by a Chlamydia bacterium, says Yang Ruifu, a soft-spoken microbiologist and a member of the team at the Academy of Military Medical Sciences (AMMS) that discovered the coronavirus.
In some few sections, coronavirus-like particles were concurrently seen. A coronavirus RNA- polymerase segment (440 bp) was amplified from the lung tissues of two cases of the SARS. After inoculated with materials from the lung samples, the similar Chlamydia-like particles were also found in the inoculated 293 cells. Since the Chlamydia-like agents visualized in both organs and cell cultures could not react with the genus specific antibodies against Chlamydia and monoclonal antibodies against C. pneumoniae and C. psittaci, the results might well be suggestive of a novel Chlamydia-like agent. Since the novel Chlamydia-like agent was found co-existing with a coronavirus-like agent in the dead cases of SARS, it looks most likely that both the agents play some roles in the disease.
https://pubmed.ncbi.nlm.nih.gov/12887816/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC421615/ (Spike Structure at the Interface between Gliding Mycoplasma mobile Cells)
https://pubmed.ncbi.nlm.nih.gov/6801766/ (Mycoplasma pneumoniae infection: role of a surface protein in the attachment organelle)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7358157/ (Concomitant infection with COVID-19 and Mycoplasma pneumoniae)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7280653/ (Outcomes of patients coinfected with COVID‐19 and Mycoplasma pneumoniae in the USA)
https://www.microbiologyresearch.org/content/journal/acmi/10.1099/acmi.0.000212?crawler=true (Mycoplasma pneumoniae co-infection with SARS-CoV-2: A case report)
https://onlinelibrary.wiley.com/doi/10.1111/ijd.15090 (COVID-19 and Mycoplasma pneumoniae: SARS-CoV-2 false positive or coinfection?)
https://covid19.researcher.life/article/covid-19-coronavirus-is-infection-along-with-mycoplasma-or-other-bacteria-linked-to-progression-to-a-lethal-outcome/6fdb83d7-fdaf-4111-965a-cea494a28613
https://link.springer.com/article/10.1007/s15010-020-01483-8 (Co-infection of SARS-CoV-2 with Chlamydia or Mycoplasma pneumoniae: a case series and review of the literature)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7437800/ (Human coronavirus OC43 infection associated pneumonia)
https://www.frontiersin.org/articles/10.3389/fmicb.2020.00685/full (Characterization of an Immunoglobulin Binding Protein (IbpM) From Mycoplasma pneumoniae)
https://www.pnas.org/content/112/16/5165 (Structure of CARDS toxin, a unique ADP-ribosylating and vacuolating cytotoxin from Mycoplasma pneumoniae)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6966865/ (Mycoplasma pneumoniae pneumonia associated thrombosis)
https://link.springer.com/article/10.1007/BF01314960 (Links and interactions between mycoplasmas and viruses: past confusions and present realities)
Before Covid there was an outbreak of MP Pneumoniae in one of Chinas military unit. I was researching/collecting all I could find about mycoplasma before Covid era. I got interested in it as soon as I read about-common mycoplasma now weaponised. Thanks for links, going to check all of them.
That's disturbing. Definitely up there on the WTF scale. Table 6 in the Shi paper is not particularly comforting. Where bad is varies by tissue type and receptor type. If it happened in mers would it happen in cov2? Well that would explain some things people have been arguing about for a good part of 2021. The whole don't count the vaxed as vaxed because lots of covid in the first 2 weeks after jab then a period of likely protection (very high end antibodies) then a decline and greater susceptibility vs unvaxed. I believe that is the arch Walter is talking about. The statisticians have been saying there is ADE on the back end for a while. Looks like they are right. The avoiding of counting people as vaccinated for 14 days post jab would be an admission that people are more vulnerable during that period as well as a way to pad the numbers on effacacy so it is undoubtably worse that presented. Table 6 seems to indicate a ramp enhancement time for MERS in all but lung DPP4 but one has to wonder about the profile for tissues not tested. Makes me wonder what the covid viral and vax antibody ramp looks like for that 14 day period. Also some of the statisticians were showing negative values against control (unvaxed) meaning vax enhanced disease after a few months using the hospital/ death and cases data. If there were a paper or two profiling antibody levels by month of recovered viral and vaxed one could swag a zone where such things may well be happening based on first 2-3 weeks and maybe about 4 months to 6 months (where the booster was then recommended) on the fist 2 jabs. The signal is strong in the vax profiles which then could be compared to the viral recovered unvaxed to see if there is a problem too. However as far as I am concerned it is enough to know there is a problem overall and to think about how to manage it for prevention, if ill and post exposure of any sort.