Covid-19 News

    Quote from JedRothwell

    As noted above, they are a threat to everyone because they may produce more dangerous variants.

    The biggest and only threat for you are the vaccinated, that get more frequent CoV-19 than the unvaccinated in case of Pfizer & Oxford/Astra. Unvaccinated present the selection criteria for new variants.

    The vaccinated also wrongly believe they are immune and need no PCR test!

    So people like you and THH spread very dangerous nonsense!


    So may be go back to school a learn basics of evolution.


    Corry about Merck-Vectin::

    Ivermectin vs Merck's new early treatment drug
    Newsmax's Host Eric Bolling interviews Dr. Pierre Kory about Ivermectin and Merck's new drug. Donate to the Front Line Covid-19 Critical Care Alliance, Inc To…
    odysee.com

    Quote from JedRothwell

    Taking ivermectin does nothing to prevent or cure COVID. You might as well take jelly beans.

    You live in fantasy land. All country statistics I analyzed show in average a ratio of 1 double vax and 4 unvaxx in ICU. So the real protection is max 4x. If you discount all people with a prior infection + vaxx then the real protection is 2x (average) Of course its higher for age <40 and much lower for age 70+...


    In your case I would be very careful if you, so far, had no infection.

    Quote from Wyttenbach

    You live in fantasy land. All country statistics I analyzed show in average a ratio of 1 double vax and 4 unvaxx in ICU. So the real protection is max 4x.



    the protection offered from the vaccine is determined by the relative probability of ending up there if vaccinated versus if not vaccinated. Defined as:


    (vaccinated in ICU / population vaccinated) / (unvaccinated in ICU / population unvaccinated)


    rearranging we get


    (vaccinated in ICU / unvaccinated in ICU) X (unvaccinated population / vaccinated population)


    Wyttenbach 1/4 (4X protection) ----------------------- Base rate ratio (Wyttenbach ignores).


    The Base rate ratio is higher in countries with high vaccination rate. It is weighted by age according to risk, so high vaccination rates for > 60 (for example) => higher base rate ratio.


    In the vaccine terror countries this base rate adjustment is particularly high. In the UK it is around 90% fully vax to 10% not fully vax or a base rate ratio factor of 1/9 - and higher than that when fully risk adjusted - the higher risk age groups are very highly vaccinated. We think. It is probably one of the reasons why Wyttenbach so misestimates vaccine protection in those countries and comes out with those ludicrous statements.


    thus if the UK had this same average 1/4 ratio it would mean a protection of better than 36X.


    Actually I do not have figures for the UK. I have this:


    Almost 90% of patients admitted to Intensive Care Units in north east London are not fully vaccinated - NHS North East London CCG
    Between July and September 2021, 203 patients with Covid-19 were admitted to intensive care units (ICU) across north east London (NEL). Of these, 90% (181)…
    northeastlondonccg.nhs.uk


    90% unvaccinated in ICU. But in the north east london vaccination levels are probably a lot lower. If it were the same as for the UK > 90%, then we have > 80X protection against ICU admission over that period.


    There are a few other issues here, correlation is not causation, but the error got from ignoring base rates is the same. Wyttenbach makes it, and other similar errors, all the time here.


    Similarly the ecological arguments that ivermectin works ignore the context (but that is a whole load of things, not just simple base rates). It is depressing there is so much bad understanding of science and maths at this most basic level.


    THH

    Quote from THHuxleynew

    (vaccinated in ICU / population vaccinated) / (unvaccinated in ICU / population unvaccinated)

    May be once try to use real UK data not a hospital of your choice. I used vaccination report 38.


    The error you do is always the same. You divide vaxx_ICU/totalvaxx what is wrong. 50% of the totalvaxx are not protected by the vaccine. These lucky people are protected by an infection. So this group size must be divided by 2!


    What normal people interests: What do I get from vaccine not from a vaccine + infection....

    The Promise of Famotidine as a Possible Low-Cost COVID-19 Treatment


    The Promise of Famotidine as a Possible Low-Cost COVID-19 Treatment
    Note that views expressed in this opinion article are the writer’s personal views and not necessarily those of TrialSite. Since the beginning of the
    trialsitenews.com


    Since the beginning of the pandemic, scientists have been wondering why some people get very sick while others don’t. The answer could relate to the responses of individuals’ mast cells to infection. Therapies to blunt their response appear to be effective, most commonly over- the- counter H2 blocker famotidine (Pepcid). Numerous observational studies suggested its effectiveness, but they garnered little attention from the medical-research establishment pecking order. Several experts started writing that mast cells may be the key, yet the National Institutes of Health (NIH) exhibited little interest. The American Association of Asthma Allergy and Immunology initially expressed interest but abruptly became disinterested. During the pandemic, the emphasis of the NIH hasn’t been on cost-effective early care to save lives but rather the allocation of what will amount to hundreds of billions to develop and distribute vaccines and exotic treatments that very well could have been complemented with low-cost pragmatic, economic medicine. Given over 700,000 deaths in the US alone—with over 44 million COVID-19 cases reported the medical research establishment’s lack of interest in economic repurposed drugs to treat COVID-19 ultimately may have cost hundreds of thousands of lives. This story highlights the potential of Famotidine and the implication of mast cells with SARS-CoV-2 disease and this author’s efforts to convince health and research agencies with money and power to listen. The good news is that the Department of Dense and an Indian pharmaceutical company are gearing up significant clinical trials.


    What is Famotidine?

    Famotidine is the generic of Pepcid, the over-the-counter heartburn drug. In addition to blocking H2 receptors on parietal cells in the stomach, it blocks H2 histamine receptors on mast cells. Mast cells are a type of white blood cell, usually associated with allergic phenomena but which respond to infection and contain many chemicals besides histamine. There are many of these cells near blood vessels and in the lungs. Unfortunately, the potential mast cell link was not appreciated initially. It took a while to realize that inflammation was the main reason most patients got so sick as the new coronavirus infection’s impacts progressed. This resulted in an obsession to find something to kill the virus.


    In prescription form (oral or IV), famotidine is used for the treatment of duodenal ulcer, gastroesophageal reflux disease (GERD), active benign gastric ulcer, and certain other conditions involving excess stomach acid. Famotidine is inexpensive, remarkably safe, easily manufactured, rapidly absorbed into the blood, and readily distributed throughout the body. Further information, including safety information about famotidine, can be found here.


    Key Discovery

    As TrialSite reported well over a year ago, Dr. Robert Malone, an internationally recognized physician-scientist and early pioneer of mRNA, first identified the potential link early on during the pandemic.


    Malone and colleagues got their start when the sequence of the novel coronavirus (now known as SARS-CoV-2) was publicly disclosed on January 10. They volunteered their time to find an antiviral treatment, knowing that successful vaccine licensure would be years away.


    Malone and colleagues applied advanced supercomputing tools to determine whether any Food and Drug Administration (FDA) licensed drugs or other nutraceuticals might be used to treat COVID-19 disease. Done voluntarily, given the emergency, Malone sought to “open source” research findings aimed at finding a potential repurposed drug treatment for COVID-19 while also demonstrating the usefulness of the system developed in support of Pentagon-based Defense Threat Reduction Agency (DTRA) rapid medical countermeasure development objectives.


    The team chose to focus on a SARS-CoV-2 virus protein that has been overlooked by many large pharmaceutical companies; a protein involved in early stages of virus replication, which also suppresses parts of the immune response to SARS-CoV-2 and other viruses. Of the top-ranked drugs identified by applying the drug discovery system developed for DTRA, the team determined that famotidine had the most attractive combination of safety, cost, and pharmaceutical characteristics. The success of the system to identify and rapidly advance a repurposed drug candidate for the treatment of COVID-19 disease has demonstrated the usefulness of the DTRA approach. Dr. Malone presented a summary of the findings and recommendations to the ASPR. The mission of the HHS Office of the Assistant Secretary for Preparedness and Response (ASPR) is to save lives and protect Americans from 21st-century health security threats.


    Based on its 3-dimensional structure, it was thought that famotidine blocked an enzyme involved with viral replication. As a result, very high doses of IV famotidine were tried in a federally funded inpatient trial later at Northwell Health. Dr. Robert Malone, mRNA vaccine pioneer, was a consultant. It looked promising, but the study was not completed, and the results were never published.


    Malone and colleagues have made a breakthrough with the combination of high-dose famotidine and celecoxib, as will be discussed later. One smaller trial’s results will be published soon, while three larger studies involving the combination are forthcoming.


    Promising Early Research

    In the May 2020 research journal, Gastroenterology, Columbia reported retrospective data on hospitalized patients treated with oral or IV famotidine suggesting a significant mortality benefit. In September, Hartford Hospital reported similar findings. At this point, people started to realize that famotidine was an H2 blocker receptor blocker on mast cells and that inflammation caused by mast cells was potentially an issue.


    In August 2020, researchers in Mississippi reported good results in ICU patients with famotidine plus cetirizine, the generic of over-the-counter Zyrtec, an H1 mast cell receptor blocker. There was a favorable report of high dose oral famotidine plus celecoxib in 25 patients in a trial that Dr. Robert Malone also advised. In January 2021, researchers in Spain reported benefits in treating infected nursing home patients with Azithromycin and various antihistamines. Antihistamines alone were beneficial as prophylaxis. Northwell Health gave 10 patients an average of 80 mg famotidine orally 3 times a day. All were much better in 48 hours. It was published in Gut, September 2020.


    Do Mast Cells Contribute to SARS-CoV-2 Cytokine Storm?

    Many mast cell experts believe that the difference between those who get sick and those who don’t is that the mast cells of those who do get sick have an abnormal response to the virus. Some of these experts suspect that this virus acts so much differently than other viruses because it can cause mast cell activation in susceptible people, with the result that mast cells signal other white cells resulting in a cytokine storm. An editorial by Dr. Theoharis Theoharides in the Annals of Allergy, Asthma and Immunology 11/5/20 suggested this. Theoharides Mast Cells and COVID


    There was an excellent review article in the November International Journal of Infectious Diseases by Dr. Lawrence Afrin. Dr. Afrin Mast Cells and COVID


    He suggested that mast cell signaling causes a cytokine storm. 17% of the population has undiagnosed mast cell activation syndrome. He said his mast cell patients, who are all on H1 and H2 blockers, never get very sick if they get COVID.


    Questions

    This author wondered why no one was doing a major COVI-19 study with over-the-counter famotidine and cetirizine. Dr. Theoharides said that luteolin and quercetin would be expected to help in mast cell stabilization. In an email on December 14, 2020, Dr. Cliff Lane, Deputy Chairman of National Institutes of Allergy and Infectious Diseases (NIAID), told me the ACTIV committee thought famotidine did not warrant a randomized trial.


    The rejection this author felt was odd to say the least. With sufficient evidence for an investigation and the fact that there were no treatments for outpatient, mild-to-moderate settings this author then sent Dr. Lane and the National Institutes of Health (NIH) antiviral expert, Dr. Dean Metcalfe, the Afrin article.


    By January 25, 2021, yours truly emailed Dr. Giselle Mosnaim, president-elect, and Dr. Mariana Castells at Brigham and Women’s, head of research for 7,000 members of the American Association of Asthma Allergy and Immunology (AAAAI). In that email, I suggested they study mast cell therapies and perform a study to determine if ivermectin’s anti-inflammatory activity was due to it being a mast cell stabilizer. Dr. Mosnaim sent back a pleasant response:


    Thank you very much, Dr. Goodkin, for bringing to our attention the role of mast cells in the cytokine storm of Covid-19 infected patients and the potential use of ivermectin. It is of critical importance to have controlled clinical trials with placebo regarding ivermectin, and I believe my hospital, the Brigham and Women’s Hospital, is considering one.


    We have a manuscript under revision indicating that patients with mast cell activation disorders, including cutaneous and systemic mastocytosis have mild Covid19 infections, and there have been no deaths, Intubations or ICU needs, indicating that mast cell activation disorders are not a risk factor for Covid19 infections or severity. More importantly, we have international collaboration with several European laboratories and have been looking at the expression of the ACE-2 receptor on mast cells and mast cells do not have the protein or the RNA for the ACE-2 receptor and cannot be infected by Covid19. It is unlikely that IL-6 is coming from mast cells currently, and we are further investigating its origin. We have a manuscript under revision with this important information.


    Best Regards


    Mariana Castells, M.D., Ph.D.


    Director Drug Hypersensitivity and Desensitization Center


    Director Mastocytosis Center


    Brigham and Women’s Hospital


    Professor of Medicine


    Harvard Medical School


    While Dr. Castells declared patients with mast cell disorders are not a risk factor for COVID, it is plausible that the mast cell therapies, which all mast cell patients are on, mitigated the severity of their response to COVID, as suggested by Dr. Afrin.


    Dr. Theoharides’ editorial shared that mast cells have ACE2 receptors, which contrasted with Dr. Castell’s point of view. Even if they don’t, they could be signaling other white blood cells via histamine or other substances as suggested by Dr. Afrin and Dr. Theoharides. Both suggested that mast cell therapies, i.e., H1 and H2 blockers, luteolin, and leukotriene inhibitors would likely be beneficial.


    A comprehensive March 2021 review article by mRNA pioneer, Dr. Robert Malone, and many others about famotidine for COVID said:


    “The most straightforward explanation of the apparent famotidine activity as a COVID-19 therapy is that the drug acts via its antagonism or inverse-agonism of histamine signaling and via its arrestin biased activation—all a result of famotidine binding to histamine receptor H2. If true, then it is reasonable to infer that a SARS-CoV-2 infection that results in COVID-19 is at least partially mediated by pathological histamine release.” Malone et al Mast cells


    Rejection

    I was notified by AAAAI that they sent my email to the Coronavirus Taskforce. Based on what I had read and understood, based on discussions with peers, and most certainly based on the dire need for any safe and effective treatment for early-onset SARS-COV-2, I expected there to be a flurry of research into mast cell therapies for COVID-19. However, by February 25, 2021, this author received an email from AAAAI declaring that Dr. Afrin’s assertions were just theories. They had no interest whatsoever. The about-face made it seem like someone had gotten to them and shut them down. Three days later, I got an email from NIH saying they were sending famotidine to the ACTIV committee for evaluation. Of course, nothing happened. I can find nothing on the AAAAI website about mast cells and COVID.


    I spoke with two American clinical investigators attempting to do trials involving famotidine. Both got no help from the NIH and abandoned the effort. A third, whose study of celecoxib and famotidine had been sponsored by the Department of Defense, could not get further funding. I was in contact with researchers in Bangladesh whose study should have been completed a long time ago but hasn’t been reported.


    Proper Study Design?

    Dr. Vikas Sukhatme at Emory, an expert in repurposed drugs, is finally doing a study in the US in outpatients but using very low doses of famotidine at 20 mg twice a day and cetirizine 10 mg once a day, doses probably too low to succeed. I am concerned that if it fails, it will be used as evidence that mast cell therapies don’t work by NIH.


    It’s been clear to me and colleagues that intentional under-dosing has been used to sabotage ivermectin in Together and ACTIV-6 where it was/is given on an empty stomach which lowers absorption 2.6 times and was or is administered 3 times a day for at least 7 days.


    High doses of famotidine are probably necessary to benefit patients with COVID i.e., 60-80 mg 3-4 times a day per Dr. Malone et al. A famotidine dose of 40 mg twice a day by prescription is commonly used in the US for GERD with few side effects. 3 of 10 patients in the Northwell outpatient study at 80 mg. 3 times a day had mild side effects. Patients with Zollinger Ellison syndrome take 160 mg 4 times a day and tolerate it well. According to poison control, it is almost impossible to die of famotidine overdose. One can get 200 20 mg famotidine from Amazon for $10.


    Emerging Studies

    This author is pleased to report that a small study to be published soon will show results. A paper coming out from the Cold Spring Harbor group for a small randomized controlled trial showed evidence statistically significant for the benefit from higher dose famotidine in COVID-19 (80 mg PO TID).


    Moreover, Dr. Robert Malone reports that three significant clinical trials will launch soon involving high dose famotidine and celecoxib. Two of these studies are supported with Department of Defense (DoD) funding, and one of the studies will be funded by an Indian pharmaceutical company. There is also a paper coming out from the Cold Spring Harbor group for a small RCT that shows statistically significant clinical benefit from high dose famotidine in COVID-19 (80mg PO TID).


    A System in Need of Reform?

    Regarding therapies to treat active COVID infection, the virus could become resistant to anything that kills it, like bacteria becoming resistant to antibiotics. Agents that nonspecifically prevent inflammation caused by the virus, like fluvoxamine, seem more likely to remain effective. Given that much if not most of the problems caused by the virus appear to be mediated via mast cells, it seems logical that using extremely cheap, safe, and effective over-the- counter drugs that Americans are familiar with, like famotidine and cetirizine, possibly with quercetin and luteolin, would be very attractive. It seems unlikely that the virus could mutate in a way that it would stimulate mast cells such that physicians could not offer a countervailing measure.


    It is extremely disappointing that over-the-counter therapies, that have a strong theoretic basis to work, that have multiple nonrandomized studies suggesting benefit, and show marked benefit in mast cell disease patients treated with them have gotten so little attention. The failure to do large, randomized trials with appropriate doses of famotidine appears purposeful on the part of NIH, consistent with their strategy of doing little to nothing with repurposed drugs. Of course, they are part of a system that aligns with industry to develop novel expensive new drugs—this by itself isn’t bad but when society pays the price with its health reform it is necessary.


    The same critique applied to the NIH goes to the specialist community. How could the allergy/immunology community not have investigated cheap, safe, over-the-counter mast cell therapies for COVID that are likely to have helped many millions all over the world?


    Famotidine Use is Associated with Improved Clinical Outcomes in Hospitalized COVID-19 Patients: A Propensity Score Matched Retrospective Cohort Study
    Background and Aims The COVID-19 pandemic has caused widespread mortality and mortality. Famotidine is commonly used for gastric acid suppression but has…
    www.medrxiv.org

    Dual-histamine receptor blockade with cetirizine - famotidine reduces pulmonary symptoms in COVID-19 patients
    The COVID-19 pandemic due to SARS-CoV-2 infection can produce Acute Respiratory Distress Syndrome as a result of a pulmonary cytokine storm. Antihistamines are…
    www.ncbi.nlm.nih.gov

    Famotidine use and quantitative symptom tracking for COVID-19 in non-hospitalised patients: a case series - PubMed
    The results of this case series suggest that high-dose oral famotidine is well tolerated and associated with improved patient-reported outcomes in…
    pubmed.ncbi.nlm.nih.gov

    Covid-19 hyperinflammation and post-Covid-19 illness may be rooted in mast cell activation syndrome - PubMed
    Hyperinflammatory cytokine storms in many severely symptomatic Covid-19 patients may be rooted in an atypical response to SARS-CoV-2 by the dysfunctional MCs…
    pubmed.ncbi.nlm.nih.gov

    COVID-19: Famotidine, Histamine, Mast Cells, and Mechanisms - PubMed
    SARS-CoV-2 infection is required for COVID-19, but many signs and symptoms of COVID-19 differ from common acute viral diseases. SARS-CoV-2 infection is…
    pubmed.ncbi.nlm.nih.gov

    Intersting interview and also: And his blog I find no fact checking against him, so he seems like a good guy. He seam to be honest and a very good source of critical thinking. His not against vaccines but he is critical of aspects how we handle them. Still the only negative posts I find about him is lacking facts so really I can't judge him from the negative side. He is also good at linking to sources. I think my ex wife who is a medical doctor soon, agrees with many of his conclusions. Personally I agree that it is weird that we do not do a cost benefit analysis and that we are risking putting young people under the bus because we have just have a focus on covid deaths e.g. mostly very old people with few years left with mostly low quality of life. On the other hand he seam to have dramatized the swedish later actions a little too much. I did not find the second wave different from the first one, in my sphere there was zero collateral damage from more stricter measures.

    Quote from THHuxleynew

    anti-vaxxer (definition)


    Somone who can't make correct real world statistical arguments.

    There are those who cannot. They are ignorant or stupid. There are others who can, but do not.

    They are evil. Tucker Carlson of FOX News is an example. He has a first-class education so I think it is likely he understands statistics. Furthermore, he has resources. He has a staff, and he could talk to just about any expert in the world. If he does not understand some particular aspect of statistics, such as the base rate fallacy, I am sure that many highly qualified experts would be happy to explain it to him.


    I have no idea which category Wyttenbach is in.

    Incoming for the disinformation crew - Pharma insiders think natural immunity is better, the vaccines are failing, and they are silent about things like myocarditis for money. I dont care what Pharma thinks, because I know the science is already here on all of the above, but now the Towne Criers must say that these Pharma insiders are part of the Covid death cult and antivaxers.


    Pfizer Scientists: ‘Your [COVID] Antibodies Are Better Than The [Pfizer] Vaccination.' #ExposePfizer - YouTube

    Quote from Navid

    Pharma insiders think natural immunity is better,

    I only watched the first three minutes.

    I'm inclined to agree with him (I'm addressing the first talker in the first minute here) that natural immunity is better than the vax, since it probably targets more proteins than just the spike.


    But he fails to mention that you have to survive the covid19 infection first (and ignore long covid) in order to get the benefit.

    Me: Since I'm in a high age-and-risk bracket I've taken the bet that the vax gives me better odds.

    Quote from Wyttenbach

    May be once try to use real UK data not a hospital of your choice. I used vaccination report 38.


    The error you do is always the same. You divide vaxx_ICU/totalvaxx what is wrong. 50% of the totalvaxx are not protected by the vaccine. These lucky people are protected by an infection. So this group size must be divided by 2!


    What normal people interests: What do I get from vaccine not from a vaccine + infection....


    You have not yet acknowledged your poor maths here (ignoring base rates).


    I'd like you to do that so others can have more confidence figures you post will not always be wrong. The base rate adjustments here are large factors - in this case 10X or more.


    Now, you are elaborating on these figures, claiming a more complex model. True, there are many other factors that can account for the raw figures apart from VE.


    However your suggestion that 50% of people in the UK have caught Coronavirus is unwarranted, even if all kept immunity. From FM1's link above what we know about natural immunity is:

    (1) even amongst diagnosed cases (not all those asymptomatic silent ones) antibody protection wanes over 8 months and 30% have no IgN response by then. 70% none by 12 months.

    (2) response is higher the more severe the infection: therefore those silent cases will have lower response, and response that lasts less long.


    Nevertheless covid infection derived immunity is a big help. So, how many people actually have it in the Uk?


    If you count silent infections obviously cases don't work. However from the ONS survey we know the ratio now of infections to cases. There are about 60% more infections than actually recorded as cases.


    If we assume that same ratio throughout the pandemic we get a total number of infections as:


    7.8M / 67.2M * 1.6 = 27%


    Those 27% will (obviously) be skewed away from the people who have been vaccinated, since once vaccinated your risk of infection goes down.


    Finally we are double counting. There is a small correction here due to the vaccinated + pre-infected group. There is a correction the other way due to the unvaccinated prior covid infection group.


    If your idea is we should all get COVID without vaccination and then be safe - just say it.


    For most of us, the risk we want to reduce is that you run when you catch COVID for the first time. Anti-vaxxers talk about natural immunity (it sounds wholesome) forgetting to mention that it comes from COVID disease, and to get lots of it you need to have got through severe COVID disease. No pain, no gain.


    In summary -

    • ignoring base rates (which W is still doing) is a 10X or more error.
    • prior infection is a small correction - a lot less than the 50% you suggest, but even that would be only a small correction in comparison with 10X base rate maths error
    • In any case prior infection reduces ICU rates for unvaccinated as well as vaccinated - and reduces those for unvaccinated more than vaccinated both because the reduction in relative risk is larger and because more unvaccinated people will have been infected than vaccinated. So without more careful analysis we cannot even say which way this adjustment will go. I suspect it is actually on the side of increasing, not reducing, the adjusted VE.


    All of these figures have second order effects which are quite difficult to quantify. You cannot simply look at raw figures and whenever you don't like them invoke second order effects without careful analysis showing them likely as large as the main effect. in this case the factor of 10X which W conveniently ignores is much larger than an optimistic factor of 1.5X from second order effects.


    I believe W is capable of doing simple maths and stats, which is why I continue with this. I think he can learn. Although, as with many anti-vaxers, he will just abandon arguments that no longer work and move onto the next bogus argument. I don't bother to correct most of them - I have limited time here. it is soul destroying and repetitive answering the antivax stuff, although as here looking in detail at the numbers always interests me.



    THH

    The official figure for prior covid infections is lower than my ballpark at 18% vs my 27% (and therefore even less kind to W).


    However, there are reasons for that which do not invalidate my figure:


    PHE monitors the proportion of the population with antibodies to COVID-19 by testing
    samples provided by healthy adult blood donors aged 17 years and older, supplied by
    the NHS Blood and Transplant (NHS BT collection). This is important in helping to
    understand the extent of spread of COVID-19 infection (including asymptomatic
    infection) in the population and the impact of the vaccine programme. 250 samples from
    every geographic region in England are tested each week using 2 different laboratory
    tests, the Roche nucleoprotein (N) and Roche spike (S) antibody assays. This dual
    testing helps to distinguish between antibodies that are produced following natural
    COVID-19 infection and those that develop after vaccination. Nucleoprotein (Roche N)
    assays only detect post-infection antibodies, whereas spike (Roche S) assays will detect
    both post-infection antibodies and vaccine-induced antibodies. Thus, changes in the
    proportion of samples testing positive on the Roche N assay will reflect the effect of
    natural infection and spread of COVID-19 in the population. Increases in the proportion
    positive as measured by S antibody will reflect both infection and vaccination. Antibody
    responses reflect infection or vaccination occurring at least 2 to 3 weeks previously
    given the time taken to generate an antibody response.
    In this report, we present the results using a 4-weekly average, of testing samples up to
    10 September 2021, which takes account of the age and geographical distribution of the
    English population. Overall, the proportion of the population with antibodies using the
    Roche N and Roche S assays respectively were 18.9% and 97.8% for the period 16
    August to 10 September (weeks 33 to 36) (Figure 3). This compares with 18.5% Roche
    N seropositivity and 97.6% Roche S seropositivity for the period of 19 July to 13 August
    (weeks 28 to 31).
    The continuing increase in seropositivity using the Roche S assay reflects the growing
    proportion of adults who have developed antibodies following vaccination. .
    Figure 4a and 4b show the proportion of the population with antibodies by age group.
    Recent increases in N seropositivity has been observed in some age groups. Roche N
    seropositivity has increased slightly in the 30 to 39 year olds from 20.2% in weeks 29 to
    32 to 21.9% in weeks 33 to 36. Similarly, small increases were observed in individuals
    aged 60 to 69 from 11.4% in weeks 29 to 32 to 13.0% in weeks 33 to 36. Roche N
    seropositivity is plateauing across all other age groups.
    The pattern of increases in Roche S seropositivity which are observed follow the roll out
    of the vaccination programme with the oldest age groups offered vaccine first (Figure
    4b). Roche S seropositivity increased first in donors aged 70 to 84 and has plateaued
    since week 13, reaching 99.3% in weeks 33 to 36.


    We know (FM1's recent post above) that IgN response from covid infection wanes over 12 months so that figure will be less than my 27% figure. In fact the two figures look about right to me. The IgN negative covid infection guys will still have some protection from IgS response (the same as the vaccine, which only delivers IgS). Of course it is all a matter of how large is that response, and it wanes over time from both vaccine and covid infection (faster from vaccine) however it is also pushed much higher initially by vaccine.

    Quote from Wyttenbach

    Our Fascist FUD'er

    Just a side comment. it is ironic, and funny, that W should call me a fascist FUDer given my political views (a bit left of centre, strongly against any form of autocracy or strong man government). And as for FUD again I am much less full of doubt than I was at the start, now we know so much more. And also less fearful: the promise of vaccines + drugs is looking pretty good for beating COVID in teh devloped world. In the young developing world, they will I guess catch COVID, but have a 10X demographic advantage over us with an effective IFR of 0.1% not 1%. Tragic if you are old there and die, but on population level it looks like just one other serious cause of mortality. Alongside malnutrition, poor access to clean water, malaria, etc, etc.

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