Special Investigation

Long-term or Prior Immunity from COVID-19

1200 Studies

COVID-19 Special

Investigation

Table of Contents

• Will recovery from COVID-19 result in long term immunity? • More research published on the lasting effects of antibodies for those recovering from infection • Immunity lasting at least 17 years? • A better strategy going forward

• What does a healthy immune response look like? The 2-Parts of the immune system

• Will infection from COVID-19 impart a lasting immune response? • Another study validates the optimistic position that T-Cell immunity from other prior coronavirus infections may provide protection from COVID-19 • Three articles and a brilliant scientist expose the levels of misinformation • Why the narrative about falling antibody levels after COVID-19 infection is NOT cause for concern • T-cells are as important as antibodies, yet frequently left out of the discussion • You can check to see if you have T-Cell protect ion from COVID-19 • Leaving important basic scientific facts out of research also seems epidemic these days • November 2020 study shows that up to 25% of people may be immune to SARS-CoV-2 without ever being infected by it • What level of population immunity will it require with SARS-CoV-2? • Evidence of lasting immunity after infection refutes the suggestion that people that have had COVID-19 need to get the vaccine • Existing immunity from previous coronavirus infections • More evidence that immunological memory to infection from the SARS-CoV-2 virus appears to be long-lasting • Majority are already immune against SARS-CoV-2 • Good news about T-cells providing certain levels of immunity from SARS-CoV-2 • A video overview of a promising study and lesson on why immunity should be lasting • My article on waning antibodies • More evidence of previous immunity providing effective resistance to SARS-CoV-2 • Another article supporting lasting immunity after recovery from COVID-19 • Government policies continue to defy the science • A new study showcases the advantage of natural infection over vaccine immunity with regard to SARS-CoV-2 variant strains • Calling out Francis Collins Director of NIH, for stating people who have had COVID-19 still need the vaccine, while citing a study suggesting that they don’t • Picture showing the various protein categories of the SARS-CoV-2 virus • Two new studies provide more evidence of lasting immunity after infection with SARS- CoV-2 • A study looking at two dozen other studies examining cross-reactivity to other coronavirus infections that provide protection against SARS-CoV-2 • Infection with other viruses may have a neutralizing effect against SARS-CoV-2. Did public lockdown measures aid in the spread of SARS-CoV-2 and thus COVID-19 disease? • The amazing duration of protection from the human immune system • Natural immunity appears to outperform vaccine immunity in the Memory Cells produced and residing in the bone marrow to release more antibodies with the next challenge from the virus • NIH provides more evidence of long-term immunity after SARS-CoV-2 infection. Why doesn’t their policy follow the science published on their own web site? • 1200 Studies- The Truth Will Prevail eBook • 1200 Studies Monthly Newsletter

Long-term or Prior Immunity from COVID-19

Will recovery from COVID-19 result in long term immunity? This is the million-dollar question that this eBook will provide an evidence-based answer to.

Seasonality of respiratory viruses As a preface for this first article, I would like to present this chart depicting the 4 human coronaviruses that have been in regular circulation over many years. This chart looks at dates from June 01, 2019 - May 01, 2020. These coronaviruses contribute to approximately 15-20% of the cases of the “common cold”. Rhinoviruses also follow a similar pattern and make up the largest percentage of the common cold viruses.

Notice that they peaked in December and decline in March and April in 2020. This is the same pattern that they follow annually. This spike also seems to follow the same pattern we are seeing with SARS-CoV-2 over these last two seasons. This “seasonality” as it is called is also true for influenza and other influenza-like illnesses caused by respiratory viruses each year.

Now we will look at a May 2020 article from Science Magazine and I will tie this into the chart we just looked at. Science Magazine published an article May 14, 2020, titled T cells found in COVID-19 patients ‘bode well’ for long-term immunity. The results reported are very encouraging for the hope for the prospects of herd immunity from the SARS-Co-V-2 virus. From the article: Immune warriors known as T cells help us fight some viruses, but their importance for battling SARS-CoV-2, the virus that causes COVID-19, has been unclear. Now, two studies reveal infected people harbor T cells that target the virus—and may help them recover. Both studies also found some people never infected with SARS- CoV-2 have these cellular defenses, most likely because they were previously infected with other coronaviruses. “This is encouraging data,” says virologist Angela Rasmussen of Columbia University. Although the studies don’t clarify whether people who clear a SARS-CoV-2 infection can ward off the virus in the future, both identified strong T cell responses to it, which “bodes well for the development of long-term protective immunity,” Rasmussen says. The more than 100 COVID-19 vaccines in development mainly focus on another immune response: antibodies. These proteins are made by B cells and ideally latch onto SARS-CoV-2 and prevent it from entering cells. T cells, in contrast, thwart infections in two different ways. Helper T cells spur B cells and other immune defenders into action, whereas killer T cells target and destroy infected cells. The severity of disease can depend on the strength of these T cell responses. Using bioinformatics tools, a team led by Shane Crotty and Alessandro Sette, immunologists at the La Jolla Institute for Immunology, predicted which viral protein pieces would provoke the most powerful T cell responses. They then exposed immune cells from 10 patients who had recovered from mild cases of COVID-19 to these viral snippets. All of the patients carried helper T cells that recognized the SARS-CoV-2 spike protein, which enables the virus to infiltrate our cells. They also harbored helper T cells that react to other SARS-CoV-2 proteins. And the team detected virus-specific killer T cells in 70% of the subjects, they report today in Cell. “The immune system sees this virus and mounts an effective immune response,” Sette says. The results jibe with those of a study posted as a preprint on medRxiv on 22 April by immunologist Andreas Thiel of the Charité University Hospital in Berlin and colleagues. They identified helper T cells targeting the spike protein in 15 out of 18 patients hospitalized with COVID-19. The teams also asked whether people who haven’t been infected with SARS-CoV-2 also produce cells that combat it. Thiel and colleagues analyzed blood from 68 uninfected people and found that 34% hosted helper T cells that recognized SARS-CoV-2. The La Jolla team detected this cross-reactivity in about half of stored blood samples collected between 2015 and 2018, well before the current pandemic began. The researchers think these cells were likely triggered by past infection with one of the four human coronaviruses that cause colds; proteins in these viruses resemble those of SARS-CoV-2. The results suggest “one reason that a large chunk of the population may be able to deal with the virus is that we may have some small residual immunity from our exposure to common cold viruses,” says viral immunologist Steven Varga of the University of Iowa. However, neither of the studies attempted to establish that people with cross reactivity don’t become as ill from COVID-19. End of article excerpts… So, essentially, because the SARS-CoV-2 virus has more similarities, It is estimated that about 20% of what we call the common cold, are caused by one of the 4 persistent coronaviruses that circulate annually. Personally, I never thought about the benefits of getting and suffering from the common cold. But now I have a whole different perspective on that. Read the rest of the article here: https://www.sciencemag.org/news/2020/05/t-cells-found-covid-19-patients- bode-well-long-term-immunity?#

More research published on the lasting effects of antibodies for those recovering from infection

This version of this study was published May 23rd, 2020 in the journal BioRxiv and titled Systemic and mucosal antibody secretion specific to SARS-CoV-2 during mild versus severe COVID-19. From the article: “When symptomatic, COVID-19 can range from a mild flu-like illness in about 81% to a severe and critical disease in about 14% and 5% of affected patients, respectively.”

“As with other coronaviruses, symptomatic SARS-CoV-2 disease causes an acute infection with activation of the innate and adaptive immune systems. The former leads to the release of several pro-inflammatory cytokines, including interleukin-6 …

Subsequently, B and T cells become activated, resulting in the production of SARS-CoV-2-specific antibodies, comprising immunoglobulin M (IgM), immunoglobulin A (IgA), and immunoglobulin G (IgG).

Whereas coronavirus-specific IgM production is transient and leads to isotype switch to IgA and IgG, these latter antibody subtypes can persist for extended periods in the serum and in nasal fluids. Whether SARS-CoV- 2-specific IgG antibodies correlate with virus control is a matter of intense discussions.”

“Interestingly, some of the SARS-CoV-2-exposed healthcare workers with negative SARS-CoV-2-specific IgA and IgG serum titers had detectable SARS-CoV-2-specific IgA antibodies in their nasal fluids and tears. Moreover, SARS-CoV-2-specific IgA levels in nasal fluids of these healthcare workers were inversely correlated with patient age.

These data show that systemic IgA and IgG production against SARS-CoV-2 develops mainly in severe COVID- 19, with very high IgA levels seen in patients with severe ARDS, whereas mild disease may be associated with transient serum titers of SARS-CoV-2-specific antibodies but stimulate mucosal SARS-CoV-2-specific IgA secretion. The findings suggest four grades of antibody responses dependent on COVID-19 severity …

We think these findings suggest a model where the extent and duration of SARS-CoV-2-related clinical symptoms, which likely correlates with virus replication, dictates the level of virus-specific humoral immunity.

This hypothesis is consistent with previous publications demonstrating that the magnitude of the humoral response toward SARS-CoV-2 is dependent on the duration and magnitude of viral antigen exposure.

Low antigen exposure will elicit mucosal IgA-mediated responses, which can be accompanied by systemic IgA production; however, systemic virus-specific IgA responses can also be absent, transient or delayed. This type of ‘mucosal IgA’ antibody response seemed to be particularly prevalent in younger individuals with mild SARS- CoV-2 infection without evidence of pneumonia.”

In another paper released May 27th, 2020 in the journal BioRxiv and titled Different pattern of pre-existing SARS-COV-2 specific T cell immunity in SARS-recovered and uninfected individuals, investigators found that people that had the SARS outbreak in 2003 have immune resistance to the latest SARS-CoV-2 virus. https://pubmed.ncbi.nlm.nih.gov/32668444/

From the Abstract: “Memory T cells induced by previous infections can influence the course of new viral infections. Little is known about the pattern of SARS-CoV-2 specific pre-existing memory T cells in human. Here, we first studied T cell responses to structural (nucleocapsid protein, NP) and non-structural (NSP-7 and NSP13 of ORF1) regions of SARS-CoV-2 in convalescent from COVID-19 (n=24). In all of them we demonstrated the presence of CD4 and CD8 T cells recognizing multiple regions of the NP protein. We then show that SARS-recovered patients (n=23), 17 years after the 2003 outbreak, still possess long-lasting memory T cells reactive to SARS-NP, which displayed robust cross-reactivity to SARS-CoV-2 NP.” Interestingly, they also found cellular immunity in COVID-19 patients that were never infected by the 2003 SARS-CoV-1 virus and believe that it is from exposure to the other common coronaviruses. This is similar to what I reported on last month from Science Magazine. https://www.sciencemag.org/news/2020/05/t-cells- found-covid-19-patients-bode-well-long-term-immunity?#

Immunity lasting at least 17 years?

An article about the May 27th study published on The Science Times online June 12th, 2020 and titled, Some Forms of Common Cold May Give COVID-19 Immunity Lasting up to 17 Years, New Research Suggests reported the following: “Immunology experts recently released a paper suggesting that coronavirus immunity might be possible through a different genetic pattern of SARS, or the common cold. They claim that this possible immunity may last up to 17 years. Coronavirus related symptoms that mimic the common cold, called betacoronavirus, may either have immunity or be infected by a milder form of the virus. Betacoronaviruses, specifically OC43 and HKU1, are the cause of common colds as well as severe chest infections, leaving the young and elderly in critical conditions. The beta virus has similar genetic features with its SARS family, such as COVID-19 and Middle East Respiratory Syndrome (MERS). If an individual had been previously exposed to the common cold, the body develops memory T cells, which become a defense system when a similar infection enters the body, resulting in immunity. T cells, a type of white blood cell, is a prominent part of the immune system, adjusting the body to respond to specific attacking pathogens. Because of their ability to create lasting shields against viruses, they are called 'memory cells.' Professor Antonio Bertoletti, an immunologist from the Duke-NUS Medical School in Singapore, and his team have new findings on the function of T cells amidst the global pandemic. They discovered that patients who survived the SARS lung virus in 2003 had immune responses to COVID-19 antibodies.

Helper T Cells 'These findings demonstrate that virus-specific memory T cells induced by betacoronavirus infection are long- lasting, which supports the notion that COVID-19 patients would develop long-term T cell immunity,' said the team. 'Our findings also raise the intriguing possibility that infection with related viruses can also protect from or modify the pathology caused by SARS-Cov-2 [the strain of coronavirus that causes COVID-19].' Four blood samples were taken from coronavirus patients who had recovered, 23 who has SARS, and 18 individuals who had exposed to neither deadly viruses. What surprised Bertoletti's team was that 50% of unexposed patients had defensive T-cells which could defend their immune system against the betacoronaviruses SARS and COVID-19. Most likely, the scientists concluded, their immunity developed memory cells from obtaining common colds caused by betacoronavirus or other unknown pathogens. https://www.sciencetimes.com/articles/26038/20200612/common-cold-give-covid-19-immunity-lasting-up- 17-years.htm

A better strategy going forward

Many have suggested that instead of quarantining the whole population, these at-risk demographics should be quarantined, and we should allow a higher percentage of the younger, healthier population to develop the infection, fight it off and then most likely have lasting natural immunity, which will then in turn protect those aged and vulnerable groups. That’s essentially what Sweden had decided to do with very good success. We should strive for natural herd immunity. It’s a beautiful thing! That is exactly what we had before vaccines for childhood diseases destroyed life-long natural herd immunity.

With COVID-19 we are finding that infection drives a very strong innate or cellular immune response, which bolsters defenses against future SARS-CoV-2 or other variations of coronavirus infection. As I reported in the July update, despite new studies calling into question the duration of the antibody response, multiple studies are now showing that the T cell response seems to last. In one study at least, that duration seems to have lasted at least 17 years.

In a paper released May 27th, 2020 in the journal BioRxiv and titled Different pattern of pre-existing SARS- COV-2 specific T cell immunity in SARS-recovered and uninfected individuals, investigators found that people that had the SARS outbreak in 2003 have immune resistance to the latest SARS-CoV-2 virus. https://pubmed.ncbi.nlm.nih.gov/32668444/

From the Abstract: “Memory T cells induced by previous infections can influence the course of new viral infections. Little is known about the pattern of SARS-CoV-2 specific pre-existing memory T cells in human. Here, we first studied T cell responses to structural (nucleocapsid protein, NP) and non-structural (NSP-7 and NSP13 of ORF1) regions of SARS-CoV-2 in convalescent from COVID-19 (n=24). In all of them we demonstrated the presence of CD4 and CD8 T cells recognizing multiple regions of the NP protein. We then show that SARS-recovered patients (n=23), 17 years after the 2003 outbreak, still possess long-lasting memory T cells reactive to SARS-NP, which displayed robust cross-reactivity to SARS-CoV-2 NP.” Interestingly, they also found cellular immunity in COVID-19 patients that were never infected by the 2003 SARS-CoV-1 virus and believe that it is from exposure to the other common coronaviruses. This is similar to what I reported on in my June newsletter from Science Magazine. https://www.sciencemag.org/news/2020/05/t-cells-found-covid-19-patients-bode-well-long-term-immunity?#

My hope is that as testing continues to expand and as a result, the number of positive cases continues to rise, we will realize that the mortality rate is much lower that originally feared (the greater number of infections compared to the deaths lowers that number). My prediction is that when those final numbers come out, the mortality rate will be significantly less than the seasonal flu. And, as those encouraging reports will be made public (if the media allows them to), it will alleviate the level of fear that has been generated, and people will have hope. And that hope will also increase the immune competency within the population. And, it will all contribute to bringing this terrible chapter in history to a close.

What does a healthy immune response look like? The 2-Parts of the immune system

The immune system consists of 2-parts. The “Innate” and the “Adaptive” portions of the immune system. The Innate immune system is the most important part of the equation to understand for this discussion. This is the part of the immune system that WE as individuals can either fortify or destroy by our daily habits and lifestyle. I will discuss later how you can optimize your Innate response through lifestyle, diet and supplementation. It is the first part of the immune system to the fight when exposed to a pathogen. It includes various types of white blood cells like phagocytes such as macrophages, mast cells, etc. and monocytes, the various neutrophils like eosinophils, basophils, dendritic cells and natural killer cells that destroy infected host cells. Then there are various proteins released by these cells, that act as cell signaling messengers coordinating the attack on an invader. All of these players team up to destroy, engulf or digest it. B cells and T (Thymus) cells both lymphocytes, have several important roles in both the Innate and Adaptive immune systems. Some of these cells are also involved in the activation of the second arm of the immune system, the Adaptive immune system. The Adaptive immune system kicks in a few days after the infection begins producing antibodies to join the fight. It is truly remarkable how all of this is orchestrated! And, if the person is exposed to the same virus at a later date, it will recognize that virus and produce antibodies to help the innate immune system fend off the attacker. Although this part of the immune system is not as influenced by lifestyle, diet and supplementation to the same extent as the Innate immune system those things are still influential. We know that just like with influenza, COVID-19 affects certain people with greater voracity. Why is that? It’s in large due to the fact that the Innate part of their immune system is compromised. This is true in the elderly, those on chemotherapy and in people with co-morbidities like obesity, diabetes and heart disease to name a few. In addition, co-morbidities of chronic disease cause high levels of systemic inflammation due to high levels of inflammatory cytokines, protein cell signaling molecules that shift the immune system towards a pro- inflammatory state, even to the point of attacking the body’s own tissues. This then predisposes those individuals to a “cytokine storm”, the of out-of-control inflammation and even the thrombosis (clotting issues), in small arteries which in some cases appears to be the cause of death. So why is only looking at antibody testing such an incomplete picture? As more is discovered about how the immune system is reacting to SARS-CoV-2 (the coronavirus that causes the disease COVID-19), we are realizing that there are other ways to gain protection other than only by the Adaptive Immune System that produces antibodies, which the COVID-19 antibody tests are limited to. We can proactively strengthen and support out Innate Immune arm of the immune system through nutritional and lifestyle actions including nutritional supplementation. That way it will be armed and ready for whatever invading presence may appear. It’s been said many times and in many contexts, the best offense is a good defense! More about that in a minute.

Will infection from COVID-19 impart a lasting immune response?

With COVID-19, we have been hearing about the large percentage of people that get infected but display little or no symptoms. This is an example of a healthy immune response. The beauty of getting the infection and fighting it off is that once you fully recover, you will have natural antibodies to help protect you from the same virus should you be exposed again. Your memory T-cells, a part of the Innate immune system will have also memorized the virus and will be ready to respond the next time it presents itself. One of the concerns we are hearing is, ”we really don’t know how long the antibody levels will last”. Or, “not everybody develops a strong antibody response”. While that may be true to some extent and under various circumstances, the fact that the immune defense is not solely dependent on antibodies is rarely discussed. In light of that, some new studies show great promise for a lasting immune response. Consider this pre-print of a study from May 27th 2020, titled Different pattern of pre-existing SARS-COV-2 specific T cell immunity in SARS-recovered and uninfected individuals:

This discussion is very important with regard to the “need” for a vaccine. And it seems as though it is one that the proponents of the COVID-19 vaccine are avoiding. It is because the vaccine works on the premise of developing an antibody response.

(Note: NP = Nucleocapsid protein, a part of the coronavirus. SARS refers to SARS-CoV-1, the first SARS outbreak from 2002-2003. Also, italicized words are mine).

Quotes from the article: • Memory T cells induced by previous infections can influence the course of new viral infections. • In all of them we demonstrated the presence of CD4 and CD8 T cells recognizing multiple regions of the NP protein. We then show that SARS-recovered patients (n=23 people), 17 years after the 2003 outbreak, still possess long-lasting memory T cells reactive to SARS-NP, which displayed robust cross-reactivity to SARSCoV-2 NP. (that number of 23 people represented 100% of those in the study that previously had a SARS-CoV-1 infection in 2003). • Thus, infection with betacoronaviruses induces strong and long-lasting T cell immunity to the structural protein NP. • These findings demonstrate that virus-specific memory T cells induced by betacoronanvirus infection are long-lasting, which supports the notion that COVID-19 patients would develop long- term T cell immunity. Furthermore, our findings also raise the intriguing possibility that infection with related viruses can also protect from or modify the pathology caused by SARS-CoV-2 infection.

If you absorb those four bulleted excerpts, you can see that this is very significant in the COVID-19 discussion regarding immunity to the infection. And especially after the amount of time elapsed for us to know and see that CoV-2 antibodies remain (and many more in memory cells stored in the bone marrow) and the T-cell response that is very robust after infection, it should provide a good rebuttal to the argument that getting a vaccine is necessary for us to move on from COVID-19. It also proves that when we consider herd immunity and the contribution to that goal by the percentage of people that have had COVID-19, we have to calculate the numbers of people that also have Innate immune protection from COVID-19, in addition to those that have a strong antibody response as part of the overall group. And it appears that that number is very significant indeed!

Realize as mentioned on the first page, that there are also four other regularly circulating human coronaviruses that have been with us for years. These four are part of one of the coronavirus species of viruses that cause symptoms of the common cold. There is also indication that past exposure to even these more benign coronaviruses could impart some protection against COVID-19.

One of the ways that this coronavirus (the SARS-CoV-2 virus) has been marketed, is by calling it a “novel” or new coronavirus. It does have some distinguishing features, but the truth is that its similarities to other coronaviruses far outweigh its differences. And that is one of the reasons why our immune system (if working properly), can have a head start against it. Yet, we really won’t know for sure for some time how long effective protection lasts from an antibody titer perspective. But one thing is for sure, if your Innate immune system is on guard and responds appropriately, you stand the best chance of sailing through it and potentially locking in a good measure of lasting protection for the future, thanks to efforts of both arms of your immune system.

Another study validates the optimistic position that T-Cell immunity from other prior coronavirus infections may provide protection from COVID-19

A study published in the journal Cell titled, Targets of T Cell Responses to SARS-CoV-2 Coronavirus in Humans with COVID-19 Disease and Unexposed Individuals, reports encouraging data about our immune system’s cross reactivity from common coronavirus infections and SARS-CoV-2. Blood samples were collected from blood banks where donors had provided the between the years 2015-2018. Those samples that were never exposed to SARS-CoV-2 showed that 40-60% of those samples demonstrated a high degree of immune reactivity to the “novel” virus that causes COVID-19. From the introduction: “Estimations of immunity are also central to epidemiological model calibration of future social distancing pandemic control measures (Kissler et al., 2020). Such projections are dramatically different depending on whether SARS-CoV-2 infection creates substantial immunity, and whether any cross-reactive immunity exists between SARS-CoV-2 and circulating seasonal “common cold” human coronaviruses.” “Based on data from SARS patients in 2003–2004 (caused by SARS-CoV, the most closely related human betacoronavirus to SARS-CoV-2), and based on the fact that most acute viral infections result in development of protective immunity (Sallusto et al., 2010), a likely possibility has been that substantial CD4+ T cell, CD8+ T cell, and neutralizing antibody responses develop to SARS-CoV-2, and all contribute to clearance of the acute infection, and, as a corollary, some of the T and B cells are retained long term (i.e., multiple years) as immunological memory and protective immunity against SARS-CoV-2 infection (Guo et al., 2020b, Li et al., 2008).”

Results: “Importantly, we utilized the exact same series of experimental techniques with blood samples from healthy control donors (PBMCs collected in the 2015–2018 time frame), and substantial cross-reactive coronavirus T cell memory was observed.” “Importantly, we detected SARS-CoV-2-reactive CD4+ T cells in ∼40%–60% of unexposed individuals, suggesting cross-reactive T cell recognition between circulating “common cold” coronaviruses and SARS-CoV- 2.” “Given the severity of the ongoing COVID-19 pandemic, it has been modeled that any degree of cross- protective coronavirus immunity in the population could have a very substantial impact on the overall course of the pandemic, and the dynamics of the epidemiology for years to come (Kissler et al., 2020).” https://www.cell.com/cell/fulltext/S0092-8674(20)30610-3

One of the most important take-aways from this and the many other studies that have found similar results, is that it is looking less and less like vaccine proponents will continue to make a case for mass vaccination. That is if they are even considering the science at all. If a significant percent of the population has had the SARS-CoV- 2 infection and possibly an even greater percentage have protection from previous encounters with either SARS-CoV-1 or other common cold coronaviruses, there may be few people that are left unprotected. And isn’t that what herd immunity is all about?! It will help protect those that are vulnerable.

Susceptibility

Then on September 23rd, 2020 at a Senate hearing hosted by the Committee on Health, Education, Labor and Pensions, Dr. Redfield the CDC Director said, “The preliminary results in the first round show that a majority of our nation, more than 90% of the population, remains susceptible”.

That statement is patently false and someone like Dr. Redfield who is at the head of the governments premier agency related to disease control has to know that. I was brought up with the understanding that a half truth is really a lie and Dr. Redfield is telling a half truth. The reason and I’m sure that those of you that have been following my newsletter from the beginning are already thinking this, is that the antibody response to SARS- CoV-2 is only half of the equation. Multiple studies released over the last 6 months have demonstrated that there is another powerful immune response against the virus that resides in the Innate Arm of the immune system, the T-cell response. The antibody response is mediated by the Adaptive Arm of the immune system. The testing being conducted by the CDC that Dr. Redfield is speaking about is antibody testing. The truth is that while there is a good way to mass test people for T-cell protection against SARS-CoV-2, it isn’t readily available to the masses. But to ignore the science that there is a very large percentage of the population who have robust T-cell protection when reporting statistics like this to legislators and the American people is disingenuous at best or an intentional misrepresentation at worst.

Additionally, the studies have also demonstrated that the amount of asymptomatic and recovered persons may be as high as 24 times greater than the number of cases we are aware of through antibody testing. Is Dr. Redfield spending any time staying current with the published literature? Is he aware that as my mother always told me, a half-truth is really a lie? What else may have been his agenda? Was he setting us up for the magical vaccine? Is he beholden to the vaccine manufacturers? These aren’t accusations, they are fair questions. These are important questions that have to be teased out and answered, because a half truth is really a lie.

Three articles and a brilliant scientist expose the levels of misinformation

Article 1- This article published in the journal Nature is a good example of what I am referring to. It is titled SARS-CoV-2- specific T cell immunity in cases of COVID-19 and SARS, and uninfected controls, and it shows definitively that there are other immune mechanisms that are protective against SARS-CoV-2 (COVID-19), other than the residual antibodies after infection. https://www.nature.com/articles/s41586-020-2550-z

From the article- “Here we studied T cell responses against the structural (nucleocapsid (N) protein) and non-structural (NSP7 and NSP13 of ORF1) regions of SARS-CoV-2 in individuals convalescing from coronavirus disease 2019 (COVID-19) (n = 36). In all of these individuals, we found CD4 and CD8 T cells that recognized multiple regions of the N protein.”

“Next, we showed that patients (n = 23) who recovered from SARS (the disease associated with SARS-CoV infection) possess long-lasting memory T cells that are reactive to the N protein of SARS-CoV 17 years after the outbreak of SARS in 2003; these T cells displayed robust cross-reactivity to the N protein of SARS-CoV-2.”

“We also detected SARS-CoV-2-specific T cells in individuals with no history of SARS, COVID-19 or contact with individuals who had SARS and/or COVID-19 (n = 37). SARS-CoV-2-specific T cells in uninfected donors exhibited a different pattern of immunodominance, and frequently targeted NSP7 and NSP13 as well as the N protein.”

Article 2- Another article published in Cell and titled, Targets of T Cell Responses to SARS-CoV-2 Coronavirus in Humans with COVID-19 Disease and Unexposed Individuals, also found that a high percentage of persons unexposed to SARS-CoV-2 (COVID-19) had T-cell responses to the disease.

From the article- “Importantly, we detected SARS-CoV-2-reactive CD4+ T cells in _40%–60% of unexposed individuals, suggesting crossreactive T cell recognition between circulating ‘‘common cold’’ coronaviruses and SARS-CoV- 2.” https://www.cell.com/cell/fulltext/S0092-8674(20)30610-3 A third article published as a pre-print in June, titled SARS-CoV-2 T-cell epitopes de¦ne heterologous and COVID-19-induced T-cell recognition,

“Cross-reactive SARS-CoV-2 T-cell epitopes revealed preexisting T-cell responses in 81% of unexposed individuals, and validation of similarity to common cold human coronaviruses provided a functional basis for postulated heterologous immunity in SARS-CoV-2 infection.” https://www.researchsquare.com/article/rs-35331/v1%20

Article 3- This article published in Science in August and titled. Selective and cross-reactive SARS-CoV-2 T cell epitopes in unexposed humans, is a wonderful reinforcement of the amazing cross reactivity of our immune system to viruses from similar families of viruses. It was created by 26 researchers from various immunology and infectious disease institutions around the U.S.

From the article- “Many unknowns exist about human immune responses to the SARS-CoV-2 virus. SARS-CoV-2 reactive CD4+ T cells have been reported in unexposed individuals, suggesting pre-existing cross-reactive T cell memory in 20 to 50% of people. However, the source of those T cells has been speculative. Using human blood samples derived before the SARS-CoV-2 virus was discovered in 2019, we mapped 142 T cell epitopes across the SARS- CoV-2 genome to facilitate precise interrogation of the SARS-CoV-2 specific CD4+ T cell repertoire. We demonstrate a range of pre-existing memory CD4+ T cells that are cross-reactive with comparable affinity to SARS-CoV-2 and the common cold coronaviruses HCoV-OC43, HCoV-229E, HCoV-NL63, or HCoV-HKU1. Thus, variegated T cell memory to coronaviruses that cause the common cold may underlie at least some of the extensive heterogeneity observed in COVID-19 disease.” https://science.sciencemag.org/content/early/2020/08/04/science.abd3871

And, one of the world’s top scientists weighs in- And lastly, in a June 04th interview by Freddie Sayers on UnHerd, Dr. Karl Friston a world-renowned biostatistician and neuroscientist believes that as many as 80% of people may not even be susceptible to the virus at all.

From the article accompanying the interview: “Professor Karl Friston, like Michael Levitt, is a statistician not a virologist; his expertise is in understanding complex and dynamic biological processes by representing them in mathematical models. Within the neuroscience field he was ranked by Science magazine as the most influential in the world, having invented the now standard “statistical parametric mapping” technique for understanding brain imaging — and for the past months he has been applying his particular method of Bayesian analysis, which he calls “dynamic causal modelling”, to the available Covid-19 data.”

“As he told me in our interview, even within the UK, the numbers point to the same thing: that the “effective susceptible population” was never 100%, and was at most 50% and probably more like only 20% of the population. He emphasises that the analysis is not yet complete, but “I suspect, once this has been done, it will look like the effective non-susceptible portion of the population will be about 80%. I think that’s what’s going to happen.”” https://unherd.com/2020/06/karl-friston-up-to-80-not-even-susceptible-to-covid-19/

How brilliant is Dr. Friston? Here is a quote from Science Magazine titled A computer program just ranked the most influential brain scientists of the modern era

When it comes to influential neuroscience research, University College London (UCL) has a lot to boast about. That's not the opinion of a human but rather the output of a computer program that has now parsed the content of 2.5 million neuroscience articles, mapped all of the citations between them, and calculated a score of each author's influence on the rest. Three of the top 10 most influential (see table below) neuroscientists hail from UCL: Karl Friston (1st), Raymond Dolan (2nd), and Chris Frith (7th). https://www.sciencemag.org/news/2016/11/computer-program-just-ranked-most-influential-brain-scientists- modern-era

Don’t the American people deserve to know about this exciting news Dr. Redfield? Dr. Fauci? Anyone? When you see most of the politicians asking Dr. Fauci and Dr. Redfield their opinion about aspects of the pandemic, it is obvious that the questions often have a partisan slant to them. But more often than not, they are demonstrating if nothing else, that most of the politicians on the hill are not well versed in science, interpreting the science and certainly about infectious disease or immunology. That allows people like Dr. Fauci and Dr. Redfield to pretty much have their way with them. But there is one Senator at least that is well read and well versed in these matters and knows that there is more to antibodies when it comes to the immune system and protection from COVID-19. And this past week Senator Rand Paul, a medical doctor himself, let Dr. Fauci know this in no uncertain terms. If you haven’t seen it, it’s a good one! Thanks Senator Paul for being a voice of reason and science when public officials try to tell half-truths.

Here is the link to that exchange: https://www.instagram.com/tv/CFr7DEMnr2R/?igshid=1kv3dfumpisur

Why the narrative about falling antibody levels after COVID-19 infection is NOT cause for concern

For some time now, there have been reports indicating that the antibody levels in people that have recovered from COVID-19 early on in the pandemic have declined. The inference is that immunity won’t be lasting. In my opinion, that is positioning and fear mongering to promote the upcoming vaccine, because according to basic immunology and other studies that couldn’t be further from the truth.

It seems as though these studies are pre-empting the release of the vaccine, attempting to create doubt in the minds of the public of the capability of their own immune systems. Setting them up so they can close the deal. Yet the narrative is fallacious, because they are not telling the whole story. And, the whole story will make people feel MUCH, MUCH better. The key and frustrating thing is how can we get the “rest of the story” as Paul Harvey used to say, out to the public at large.

The latest study came from the Imperial College of London titled, Declining prevalence of antibody positivity to SARS-CoV-2: a community study of 365,000 adults. https://www.imperial.ac.uk/media/imperial- college/institute-of-global-health-innovation/MEDRXIV-2020-219725v1-Elliott.pdf

Before I go any further, does that group sound familiar? Yes, it’s the same group that gave us the fatal and flawed predictions that set the world on fire over COVID-19. The same group that predicted 2.2 million deaths in the U.S. The same group responsible for driving the panic and subsequently the lockdowns. The same group of which the infamous Neil Ferguson belongs, making that prediction and the same Neil Fergusson a decade earlier was involved with the Swine Flu predictions that turned out essentially to be a hoax. Ferguson predicted global deaths would be four million. The worldwide total turned out to be 18,500. In 2005, Ferguson said that up to 200 million people could die from bird flu. Between 2003 and 2009, just 282 people died worldwide from the disease. Furthermore, this is the same group that is funded by Bill Gates. Ferguson is a panic driving mouthpiece for Gates and pharma.

So, in the study the researchers documented the decline of antibodies to SARS-CoV-2 in various groups.

Here are the results: (I have formatted the results to make them easier to separate the groups, with my comments in red)

“There were 17,576 positive tests over the three rounds.

• Antibody prevalence, adjusted for test characteristics and weighted to the adult population of England, declined from 6.0% [5.8, 6.1], to 4.8% [4.7, 5.0] and 4.4% [4.3, 4.5], a fall of 26.5% [-29.0, -23.8] over the three months of the study.

• There was a decline between rounds 1 and 3 in all age groups, with the highest prevalence of a positive result and smallest overall decline in positivity in the youngest age group (18-24 years: -14.9% [-21.6, -8.1]), (this makes sense because younger people’s immune systems are more resilient. And, it may also reflect that they are mixing in the community more than elderly and getting natural “boosting” of antibodies)

• and lowest prevalence and largest decline in the oldest group (75+ years: -39.0% [-50.8, -27.2]); (this also makes sense because younger people’s immune systems are more resilient)

• there was no change in antibody positivity between rounds 1 and 3 in healthcare workers (+3.45% [- 5.7, +12.7]).” (this makes sense because healthcare workers have intermittent exposure to the virus and that gives them that natural booster of antibody production)

They did make a brief mention about T-cell immunity, albeit insignificant and not helpful: “In addition it is currently not clear what contribution T cell immunity and memory responses will play in protective immunity during re-exposure. As such, it is not possible to say with certainty that the loss of antibody positivity in the LFIA would correlate with an increased risk of an individual being reinfected.”

In my opinion, it is disingenuous for them to say …”it is currently not clear what contribution T-cell immunity and memory responses will play….” First of all, there are numerous studies that they could have referred to showing strong T-cell responses to SARS-CoV-2. I have covered many of these in previous issues. And secondly, memory cells and their role in infection are a basic biology and immunology tenant, taught medical and chiropractic students for decades. Memory cells are B-cells that lie dormant, waiting for the same virus to arouse them, at which point they become antibody factories once again. They are not even taking this into account in this study, other than this very brief mention.

T-cells are as important as antibodies, yet frequently left out of the discussion

In an article published in nymag.com August 9th 2020, titled The Good News About T-Cells and Herd Immunity, the author David Wallace-Wells said the following: “When I asked Eric Topol, the head of Scripps, whether it was a plausible hypothesis that T-cell immunity could significantly protect you from severe disease, he replied, “Yeah, oh yeah!” He told me he’d been tested for T-cell response — not all that easy for most of the public — “and I was wishing, when I had my test, that I had it, so I’d have a fighting chance if I get [the virus], when I get it.” T-cell cross-immunity, he said, “is very likely playing a significant role. Why are some people asymptomatic? Why do some people who get the infection have such a mild response — so mild they hardly get sick? Is it because of the T-cell activation? I think it’s part of this story. It may even be the main explanation of why people never develop symptoms, or why they might have such mild symptoms.” He added, “That’s a leading hypothesis for sure.” At the population level, he said, “When only antibody data are presented, we are missing a very big part of the story.”” https://nymag.com/intelligencer/amp/2020/08/reasons-for-covid-19-optimism-on-t-cells-and-herd-immunity.html

You can check to see if you have T-Cell protection from COVID-19

T-Detect is a company that offers testing for presence of T-Cell immunity for COVID-19. Order the blood draw kit. Take it to a lab to perform your blood draw and ship the sample to the T-Detect lab. You can access that kit here. https://www.t-detect.com/ . The cost is $159.

Leaving important basic scientific facts out of research also seems epidemic these days

Giving the media fodder to run with that pumps up the vaccine narrative seems to be all too commonplace during this pandemic. Here is what I mean by that.

A Web MD article had the following quote: “The findings are a blow to scientists who think herd immunity will eventually bring down the coronavirus.” https://www.webmd.com/lung/news/20201028/covid-19-antibodies-decline-over-time-study-says

Again, another example of stoking the fires of misinformation. Herd immunity does not depend on active antibodies alone as I will share in a moment. But also, to make this sound like a surprise “blow” to scientists. What scientists exactly are they referring to? Certainly not ones that study or are trained in immunology. Or scientists that have done their homework.

In our lymphatic nodes there are follicular dendritic cells that pick up the antigens that are washing into the lymph nodes from the tissues and present them to the dormant or memory B-cells. The B-cells then determine if they can bind with this antigen. This is called “affinity maturation”. This “trains” the B-cells to make more effective antibodies. Therefore, we don’t even need as many antibodies to handle the pathogen, because they are more efficient and more effective. According to Dr. Mobeen, their antibodies “their antibodies are actually going to be better quality than the B-cells in the beginning.” That mean the antibody response will be even more effective that of the original antibodies.

Dr. Syed Mobeen lecture on declining antibodies: https://www.youtube.com/watch?v=ShvfAmlguC0 For the immune overview of this episode and why we don’t have to worry about declining antibodies, you can shortcut to 9 minutes and watch the rest from there…

Another key component is the function of the Innate Arm of the immune system and its ability to fight the infection from the very onset of exposure. We have T-cells called Natural Killer (NK) cells that can help from the start. They have combined with CD8+ and are also referred to as Cytotoxic T-cells. They can directly kill the harmful pathogens or in the case of cancer, the cancer cells. Children have higher levels of NK cells and this is one of the reasons that have been hypothesized as to why their cases are typically so mild and short.

We also have T-cells that in the presence of CD4+ become Helper T-cells. They help the other parts of the immune system determine how to respond.

A great example of this response is portrayed in an article titled, Intrafamilial Exposure to SARS-CoV-2 Induces Cellular Immune Response without Seroconversion.

The conclusion from the abstract sums it up nicely: “Exposure to SARS-CoV-2 can induce virus-specific T cell responses without seroconversion. T cell responses may be more sensitive indicators of SARS-Co-V-2 exposure than antibodies. Our results indicate that epidemiological data relying only on the detection of SARS-CoV-2 antibodies may lead to a substantial underestimation of prior exposure to the virus.”

So, it is possible for some people with strong innate immunity to fight off SARS-CoV-2 without any significant levels of antibodies. These are the ones that are being called the asymptomatic cases. And they account for a large percentage of the infections, especially in children and young people. Although as a result of the infection, the B-cells will also produce antibodies.

Another study to check out was published in Nature July 29th, 2020 titled SARS-CoV-2-reactive T cells in healthy donors and patients with COVID-19. They wanted to see the levels of these immune cells in people that had COVID-19 and the people that have not and haven’t been exposed. A percentage of the population already has some immunity to SARS-C0V-2, based on their prior exposure to seasonal coronaviruses that make up about 20% of the common colds that people suffer from.

From the study: “Here we investigated CD4+ T cells that are reactive against the spike glycoprotein of SARS-CoV-2 in the peripheral blood of patients with COVID-19 and SARS-CoV-2-unexposed healthy donors. We detected spike- reactive CD4+ T cells not only in 83% of patients with COVID-19 but also in 35% of healthy donors.”

The average age of patients with COVID-19 was 52.6 years and the average age of the unexposed healthy donors was 41.9 years. It would be interesting to see what the percentage these cells would be present in healthy unexposed young children and even young adults. https://www.nature.com/articles/s41586-020-2598-9

As a closing thought. There have been only a handful of suspected re-infections world-wide and some of those have been brought into question. With over 45 million CV-19 confirmed infections to date, wouldn’t you think there would be tens or hundreds of thousands of reinfections if waning antibodies really put us at risk. Just food for thought .

November 2020 study shows that up to 25% of people may be immune to SARS- CoV-2 without ever being infected by it

I have covered many studies over the last 6 months that reveal encouraging signs that T-Cell cross-reactivity from other coronavirus infections provides a significant amount of immunity against SARS-CoV-2 for many people. Here is another recent release with similar findings.

The study pre-print released November 04, 2020 and titled, SARS-CoV-2 responsive T cell numbers are associated with protection from COVID-19: A prospective cohort study in keyworkers, gives major insights and perspective on the real mortality rates from COVID-19.

According to an article published in The Sun Tmes (U.K.): Dr Peter Wrighton-Smith, the CEO of Oxford Immunotec, the company that developed the T-cell test for trial, said that the results show that relying on antibody testing alone to see who is immune to the virus could underestimate the number of people who have immunity. Data from the study found that none of the participants with high T-cell responses became infected with the virus in the following four months. Commenting on the results Dr Wrighton-Smith said the people used in the study had all been frontline workers and were therefore more likely to have been exposed to the virus. He said: “The implication is that there is a population of people who are protected from Covid who are not being picked up by the antibody studies.” The experts stressed that the findings could mean that T-cells are longer lasting than antibodies or that people are left with immunity after suffering from similar coronaviruses such as the common cold. Dr Wrighton-Smith added: “We are not picking up all cases with the antibody surveys - so more people may be protected than we thought.” The lead author of the study, Dr David Wyllie, a consultant microbiologist at PHE said that just four months into the study, 20 of the participants had lower T-cell responses and had developed Covid, in comparison none of the individuals with high T-cell responses contracted the virus. He said: “This suggests individuals with higher numbers of T-cells recognising SARS-CoV-2 may have some level of protection from Covid-19, although more research is required to confirm this.” Reacting to the publication of the study, Professor Karol Sikora, a cancer expert at the University of Buckingham said the finding was “really good news”.

From the study: Methods: We conducted a prospective cohort study in 2,826 participants working in hospitals and Fire and Police services in England, UK during the pandemic (ISRCTN5660922). Of these, 2,672 were unselected volunteers recruited irrespective of previous SARS-CoV-2 RT-PCR test results, and 154 others were recruited separately specifically because they previously tested positive.

Results: T cells responsive to the spike (S), nuclear (N) and membrane proteins (M) dominated the responses measured. Using the sum of the spots (responsive cells within each well of 250,000 peripheral blood mononuclear cells) for S, N and M antigens minus the control, the 2,672 unselected participants were divided into those with higher responses (n=669, 25.4%; median 30 spots (IQR 18,54)) and those with low responses (n=2016, 76.7%, median 3 (IQR 1,6)), the cutoff we derived being 12 spots. Of the participants with higher T cell responses, 367 (53%) had detectable antibodies against the N or S proteins. During a median of 118 days follow-up, 20 participants with lower T cell responses developed COVID-19, compared with none in the population with high T cell responses (log-rank test, p=6x10-3). Conclusions: Peripheral blood SARS-CoV-2 responsive T cell numbers are associated with risk of developing COVID-19.

Discussion: Overall, this study suggests that serology may underestimate the working age population at lower risk of clinical SARS-CoV-2 infection, something which might impact outbreak kinetics (29) and which has been suspected on epidemiological grounds (30). We would speculate that the declining number of individuals with high levels of SARS-CoV-2 responsive T cells with increasing age may explain higher illness incidence and severity in older age (1-4). Intriguingly, our data indicate individual level risk stratification may be possible using T-cell assays, including the standardised assay kits used in this study which, being in the same format as the widely used T-SPOT®.TBtests for latent TB infection, would be readily deployable at scale https://www.medrxiv.org/content/medrxiv/early/2020/11/04/2020.11.02.20222778.full.pdf

Considering all of that…

What level of population immunity will it require with SARS-CoV-2?

The R-Naught (R0 or Basic Reproduction Number) for an infectious disease event is the estimated number of people that an infected person will in turn infect. It is generally reported as a single numeric value or low–high range. An outbreak is expected to continue if R0 has a value >1 and to end if R0 is <1. It also is used to estimate the percentage of the population that would need to be “immune” from a disease to control its spread through the concept of herd or population immunity. The more infective the disease, the higher the percentage of the population would need to be immune. Measles for example is estimated to have an R0 somewhere between 12-18. Therefore, it is thought that the percentage of the population that would need to be immune to protect the rest would be around 90-95%. A virus with an R0 of 2-3 may only require 60% of the population to be immune to control the outbreak.

The R0 for the SARS-CoV-2 virus is estimated to be 2.5, as of the last published data from the CDC in August. As an infection works its way through the population that number will be expected to drop. The R0 for the seasonal flu ranges from 0.9-2.1. The common cold is estimated to be 2-3. Even with an infectibility rating near that of SARS-CoV-2, not everyone contracts the seasonal flu or the common cold each year. And, as larger numbers of the population become infected and recover, the number of susceptible hosts drop and the likelihood of getting infected drops. Eventually the virus “burns itself out”. That is what happened to SARS- CoV-1. A vaccine was never successfully developed and in fact the effort was abandoned because the trials never went beyond animal studies. The vaccine candidates caused severe adverse effects in the animal subjects and the efforts were dropped.

Evidence of lasting immunity after infection refutes the suggestion that people that have had COVID-19 need to get the vaccine

*The following articles are in addition to the many studies I have posted over the last several months in my update newsletter.

Reports of “waning antibodies” are a false flag and not a cause for concern

Giving the media fodder to run with that pumps up the vaccine narrative, seems to be all too commonplace during this pandemic especially now that the vaccines are here, and the push is on (pun intended). More than ever, leaving important and basic scientific facts out of reporting is epidemic these days. Here is what I mean by that.

A Web MD article titled, COVID-19 Antibodies Decline Over Time, Study Shows, had the following quote: “The findings are a blow to scientists who think herd immunity will eventually bring down the coronavirus.” https://www.webmd.com/lung/news/20201028/covid-19-antibodies-decline-over-time-study-says

Again, another example of stoking the fires of misinformation. Herd immunity does not depend on active antibodies alone as I will share in a moment. But also, to make this sound like a big surprise, or “blow” to scientists is ridiculous. What scientists exactly are they referring to? Certainly not ones that study or are trained in immunology. Or, the scientists that have done their homework.

In our lymphatic nodes there are what are called follicular dendritic cells. These cells pick up the antigens that are washing into the lymph nodes from the tissues and present them to the dormant (like sleeping) or memory B-cells. The B-cells then determine if they can bind with this antigen. It’s like a handshake of recognition. This is called “affinity maturation”. This “trains” the B-calls to make more effective antibodies. Therefore, with future infections with the same virus we don’t even need as many antibodies to handle the pathogen, because they are more efficient and more effective than the first exposure antibodies. According to Dr. Mobeen Syed, “their antibodies are actually going to be better quality than the B-cells in the beginning.”

Dr. Mobeen Syed’s lecture on declining antibodies can be found here: https://www.youtube.com/watch?v=ShvfAmlguC0 For the immune overview of this episode and why we don’t have to worry about declining antibodies, you can shortcut to 9 minutes and watch the rest from there…

Another key component is the function of the Innate Arm of the immune system and its ability to fight the infection from the very onset of exposure. We have T-cells called Natural Killer (NK) cells, as well as others that can help from the start. They combine with CD8+ and are also referred to as Cytotoxic T-cells. They can directly kill the harmful pathogens or in the case of cancer, the cancer cells. Children have higher levels of NK cells and this is one of the reasons hypothesized as to why their cases of COVID-19 are typically so mild and short.

As a general overview, we also have T-cells that in the presence of CD8+ glycoprotein become Cytotoxic lymphocytes. They kill infected cells and cancer cells. And, T-cells in the presence of CD4+ glycoprotein become Helper T-cells, which help the other parts of the immune system determine how to respond. So T-cell immune response is a major player, that for some strange reason seems to elude the discussions that focus on antibodies and vaccines.

A great example of this type of response is portrayed in an article titled, Intrafamilial Exposure to SARS-CoV-2 Induces Cellular Immune Response without Seroconversion.

Existing immunity from previous coronavirus infections

There have been only a handful of suspected re-infections world-wide despite 76 million cases to date. And, there are various questions about whether those were true cases of reinfection. With nearly 18 million confirmed COVID-19 infections to date in the U.S., wouldn’t you think there would be tens or even hundreds of thousands of reinfections if waning antibodies really put us at risk? Just food for thought.

As a closing thought. Back to the lead article in this story from Web MD. The study that article was based on came out of The Imperial College London, the same folks that brought us the Neil Ferguson debacle that led to the crushing lockdowns in the first place. Professor Ferguson, (another Bill Gates fundee), used faulty modeling to predict that 2.2 million Americans and over 500,000 people in the UK would die from COVID-19. This set the world into a panic leading to a level of fear and hysteria that the world has never seen and most certainly contributing to the tremendous death toll at the start of the pandemic, the collateral damage from the extended lockdowns and the inhumane policies of separating sick and dying people from their loved ones.

We must be on guard against research and reporting that is agenda driven. Be a healthy skeptic. Question everything. Look for false flags. Dissect the author’s possible bias and conflicts of interest, the data, the conclusions and the possible motivation behind the results.

More evidence that immunological memory to infection from the SARS-CoV-2 virus appears to be long-lasting

A pre-print article posted November 16th 2020 titled, Immunological memory to SARS-CoV-2 assessed for greater than six months after infection, supports the growing scientific consensus that immunity after infection with SARS-CoV-2 is will be long-lasting.

From the abstract Understanding immune memory to SARS-CoV-2 is critical for improving diagnostics and vaccines, and for assessing the likely future course of the pandemic. We analyzed multiple compartments of circulating immune memory to SARS-CoV-2 in 185 COVID-19 cases, including 41 cases at > 6 months postinfection. Spike IgG was relatively stable over 6+ months. Spike-specific memory B cells were more abundant at 6 months than at 1 month. https://www.biorxiv.org/content/10.1101/2020.11.15.383323v2

Majority are already immune against SARS-CoV-2

An excellent article from Mercola.com titled, Majority are already immune to SARS-CoV-2 covers several different aspects showing lasting immunity after infection and that a high percentage of the population already have immunity against COVID-19 disease.

Story at a glance Several studies suggest immunity against SARS-CoV-2 infection is far more widespread than anyone imagined, and that the threshold for herd immunity is far lower than previously estimated.

• German research shows that even among unexposed individuals, 81% were resistant or immune to SARS-CoV-2 infection.

• Common colds caused by the betacoronaviruses OC43 and HKU1 might make you more resistant to SARS-CoV-2 infection.

• If a majority already have some measure of immunity against COVID-19 due to previous exposure to other coronaviruses, then we've probably already reached the threshold for herd immunity and vaccinating every human on the planet is unnecessary.

• Several studies suggest the herd immunity threshold is well below 50%, according to one study, as low as 9%. Meanwhile, a mathematical model suggests immunity against SARS-CoV-2, globally, might be as high as 80%. https://articles.mercola.com/sites/articles/archive/2020/10/14/herd-immunity-coronavirus.aspx

Good news about T-cells providing certain levels of immunity from SARS-CoV-2

An article scheduled to be released in January 2021 in the Journal Nature Immunology and titled, SARS-CoV-2- derived peptides define heterologous and COVID-19-induced T cell recognition, provides some shocking revelations about pre-existing immunity to SARS-CoV-2 from previous infections by its distant cousins, the 4 human coronaviruses making up part of the common cold spectrum. https://www.nature.com/articles/s41590-020-00808-x

A video overview of a promising study and lesson on why immunity should be lasting

Dr. Mobeen Syed is a medical professor of immunology and his Drbeen Medical Lectures COVID-19 podcast host that I have been following and have learned a tremendous amount from. This is from an episode he did that was an excellent lesson on the subject. The antibodies at 6 months post infection are more mature and responsive in case of re-exposure to the virus down the road. You can find it on his YouTube channel. It is titled, Study- Antibody Immunity to SARS-CoV-2 lasts and matures at 6 months and can be accessed here. https://www.youtube.com/watch?v=lxdF3Hv7nQQ

My article on waning antibodies

Reports of “waning antibodies” are a false flag and not a cause for concern

Again, another example of stoking the fires of misinformation. Herd immunity does not depend on active antibodies alone as I will share in a moment. But also, to make this sound like a big surprise, or “blow” to scientists is ridiculous. What scientists exactly are they referring to? Certainly not ones that study or are trained in immunology. Or the scientists that have done their homework.

So, what is normal with any infection? Normal is that antibodies are produced…IgG, IgM and IgA to name the more common ones (Ig stands for Immunoglobulin). These immunoglobulins or antibodies ramp up to fight the infection, but then they also NORMALLY decline once the threat is past. In fact, if they didn’t it could lead to other immune related problems as a result. In the SARS-CoV-2 infection, the IgM declines first followed later by the IgG levels.In our lymphatic nodes there are what are called follicular dendritic cells. These cells pick up the antigens that are washing into the lymph nodes from the tissues and present them to the dormant (like sleeping) or memory B-cells. The B-cells then determine if they can bind with this antigen. It’s like a handshake of recognition. This is called “affinity maturation”. This “trains” the B-calls to make more effective antibodies. Therefore, with future infections with the same virus we don’t even need as many antibodies to handle the pathogen, because they are more efficient and more effective than the first exposure antibodies. According to Dr. Mobeen Syed, “their antibodies are actually going to be better quality than the B-cells in the beginning.”

Another key component as I have mentioned is the function of the Innate Arm of the immune system and its ability to fight the infection from the very onset of exposure. Let’s look a little closer at that. We have T-cells called Natural Killer (NK) cells, as well as others that can help from the start. They combine with CD8+ and are also referred to as Cytotoxic T-cells. They can directly kill the harmful pathogens or in the case of cancer, the cancer cells. Children have higher levels of NK cells and this is one of the reasons hypothesized as to why their cases of COVID-19 are typically so mild and short.

As a general overview, we also have T-cells that in the presence of CD8+ glycoprotein become Cytotoxic lymphocytes. They kill infected cells and cancer cells. And, T-cells in the presence of CD4+ glycoprotein become Helper T-cells, which help the other parts of the immune system determine how to respond. So T- cell immune response is a major player, that for some strange reason seems to elude the discussions that focus on antibodies and vaccines.

A great example of this type of response is portrayed in an article titled, Intrafamilial Exposure to SARS-CoV-2 Induces Cellular Immune Response without Seroconversion.

More evidence of previous immunity providing effective resistance to SARS-CoV-2

Another article supporting lasting immunity after recovery from COVID-19

Another article published in Science January 6th, 2021 titled Immunological memory to SARS-CoV-2 assessed for up to 8 months after infection, found robust defenses up to 8 months post infection. This adds to the numerous articles I have presented over the last several month suggesting that protective immunity may even last several years. From the Concluding Remarks:

In this study, we aimed to fill gaps in our basic understanding of immune memory after COVID-19. This required simultaneous measurement of circulating antibodies, memory B cells, CD8+ T cells, and CD4+ T cells (CD8+ are Cytotoxic “killer” T-cells, CD4+ are Helper T-cells), specific for SARS-CoV-2, in a group of subjects with a full range of disease, and distributed from short time points after infection out to 8 months later. By studying these multiple compartments of adaptive immunity in an integrated manner, we observed that each component of SARS-CoV-2 immune memory exhibited distinct kinetics. Biologically, IgG antibodies having a half-life of ~21 days, and the magnitude of the antibody response over time reflects antibodies produced first by short-lived plasma cells and then long-lived plasma cells, with affinity maturation (These “Sleeper” cells are trained while they sleep for faster and stronger response and activated when an infection by the virus occurs later. I discussed this in detail in the November issue of this newsletter), also impacting the apparent magnitude in conventional binding assays and neutralization assays. Overall, at 5 to 8 months PSO (PSO is Post Symptom Onset), almost all individuals were positive for SARS-CoV-2 Spike and RBD IgG. (RBD is Receptor Binding Domain) Notably, memory B cells specific for the Spike protein or RBD were detected in almost all COVID-19 cases, with no apparent half-life at 5 to 8 months post-infection. (no apparent half-life meaning they didn’t reduce 50%) Antibodies are the only component of immune memory that can provide truly sterilizing immunity…… In human COVID-19 infections, SARS-CoV-2-specific CD4+ T cells and CD8+ T cells are associated with less COVID-19 disease severity during an ongoing SARS-CoV-2 infection (5). Rapid seroconversion was associated with significantly reduced viral loads in acute disease over 14 days (29). Both of those associations are consistent with the hypothesis that SARS-CoV-2 memory T cells and B cells would be capable of substantially limiting SARS-CoV-2 dissemination and/or cumulative viral load, resulting in reduced COVID-19 disease severity. The likelihood of such outcomes is also closely tied to the kinetics of the infection, as memory B and T cell responses can take 3-5 days to successfully respond to an infection. As noted above, given the relatively slow course of severe COVID-19 in humans, resting immune memory compartments can potentially contribute in meaningful ways to protective immunity against pneumonia or severe secondary COVID-19. The presence of sub-sterilizing neutralizing antibody titers at the time of SARS-CoV-2 exposure would blunt the size of the initial infection, and may provide an added contribution to limiting COVID-19 severity, based on observations of protective immunity for other human respiratory viral infections (37, 72– 74) and observations of SARS-CoV-2 vaccines in non-human primates (48, 67, 75). Nevertheless, our data show immune memory in at least three immunological compartments was measurable in ~95% of subjects 5 to 8 months PSO, indicating that durable immunity against secondary COVID-19 disease is a possibility in most individuals. End of excerpts:

Government policies continue to defy the science

And, in case there was any doubt whether our own health agencies are monitoring this good news here is a screen capture from a summary of this study on the NIH web site.

See graphic next page… https://www.nih.gov/news-events/nih-research-matters/lasting-immunity-found-after-recovery-covid-19

From the article The researchers found durable immune responses in the majority of people studied. Antibodies against the spike protein of SARS-CoV-2, which the virus uses to get inside cells, were found in 98% of participants one month after symptom onset. As seen in previous studies, the number of antibodies ranged widely between individuals. But, promisingly, their levels remained fairly stable over time, declining only modestly at 6 to 8 months after infection. (My comment: The decrease in antibodies over time is a NORMAL immunological response recognized for decades [It is rooted in Immunology 101 courses]. Once the threat is gone, there is no reason to continue to make antibodies at the same level as during active infection. Thankfully the memory B and T cells that reside in the bone marrow continue to mature with subtle exposures (called affinity maturation). Later when faced with a threat from that virus in the future, these memory cells kick out copious levels of new antibodies and T-cells to work to neutralize the new exposure. This type of immunological memory is often known to last several decades https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1885547/ and https://pubmed.ncbi.nlm.nih.gov/12925846/ ) Virus-specific B cells increased over time. People had more memory B cells six months after symptom onset than at one month afterwards. Although the number of these cells appeared to reach a plateau after a few months, levels didn’t decline over the period studied. Levels of T cells for the virus also remained high after infection. Six months after symptom onset, 92% of participants had CD4+ T cells that recognized the virus. These cells help coordinate the immune response. About half the participants had CD8+ T cells, which kill cells that are infected by the virus. As with antibodies, the numbers of different immune cell types varied substantially between individuals. Neither gender nor differences in disease severity could account for this variability. However, 95% of the people had at least 3 out of 5 immune-system components that could recognize SARS-CoV-2 up to 8 months after infection. “Several months ago, our studies showed that natural infection induced a strong response, and this study now shows that the responses last,” Weiskopf says. My comment: Unfortunately, you would never know that they are keeping up with the science by the nonsensical policies they are making, like recommending people that have recovered from COVID-19 still get vaccinated and risk vaccine adverse effects unnecessarily. It is ironic that as you can see from the screen capture above, the section of the NIH website this story came from is their “Research Matters” section. Does it really? Unless that research turns into policy decisions that will make a difference in the big picture, does it really matter?

A new study showcases the advantage of natural infection over vaccine immunity with regard to SARS-CoV-2 variant strains

As a great follow up on the previous discussion on natural immunity, a new pre-print study titled Memory B cell repertoire for recognition of evolving SARS-CoV-2 spike highlights the effectiveness of long-term capabilities, diversity and flexibility of memory immune function. From the abstract: Memory B cell reserves can generate protective antibodies against repeated SARS-CoV-2 infections, but with an unknown reach from original infection to antigenically drifted variants. The results furnish a global atlas of the S-specific memory B cell repertoire and illustrate properties conferring robustness against emerging SARS-CoV-2 variants. More from the study: (PC = Plasma Cells, GC = Lymphoid tissue Germinal Centers, ABs = Antibodies and SHM = gene Somatic Hyper- Mutation) Both PC-derived secreted antibody and memory B cells supply immune memory to prevent repeat infection, but with non-redundant roles. Secreted antibodies can prophylactically thwart pathogen invasion with fixed recognition capability, while memory B cells harbor expanded pathogen recognition capacity and can differentiate quickly into PCs to contribute dynamically to the secreted antibody repertoire (4). Moreover, memory B cells retain plasticity to adapt to viral variants through GC re-entry and SHM-mediated evolution (5). In a comprehensive competition analysis of 152 monoclonal antibodies (mAbs) from 19 subjects for binding with trimeric S ectodomain, we have identified 7 recurrently targeted competition groups -- three for antibodies with epitopes on the receptor-binding domain (RBD), two for epitopes on the N-terminal domain (NTD), and two for S2 epitopes. We show that these groups represent the major practical antibody footprints, with rare antibodies outside them. Discussion: Our results illustrate the landscape of memory B cell coverage of the SARS-CoV-2 S glycoprotein in convalescent donors. Unlike the terminally differentiated plasma cells that determine the profile of serum antibodies, memory B cells will clonally expand upon re-exposure to antigen, some differentiating into fresh antibody secreting cells and others re-entering germinal centers and undergoing further SHM-mediated diversification and affinity maturation. These outcomes offer a layer of flexibility for adaptation to drifted or related viral strains, if available secreted antibodies fail to prevent initial infection. Loss of protection against overt or severe disease is not an inevitable consequence of a waning serum antibody titer. This atlas of B cell memory therefore maps systematically a crucial component of the long-term immune response to SARS-CoV-2 infection. Complementary recognition of non-overlapping viral targets by non-competing antibodies in the repertoire can reduce the likelihood of viral escape (41). Our data suggest an additional mechanism for preventing viral escape: competing antibodies may help retain recognition of a rapidly evolving antigen by their differential sensitivity to specific mutations. The potential dynamic reach of otherwise redundant mAb recognition, illustrated by selective retention of affinity for the UK variant by some antibodies within a cluster but not by others, may give selective advantage to immune mechanisms that yield multiple competing antibodies to critical epitopes, as those that retain adequate affinity can then re-activate, expand, and potentially undergo further affinity maturation. The emergence of strains that may have gained selective advantage by escape from neutralization emphasizes the importance of determining whether the level of retained affinity for the S protein by some antibodies in the immunodominant clusters influences protection from clinical disease. https://europepmc.org/article/MED/33758863

Calling out Francis Collins Director of NIH, for stating people who have had COVID-19 still need the vaccine, while citing a study suggesting that they don’t

In a February 23rd, 2021 article written by Francis Collins in The Director’s Blog on the NIH website, Dr. Collins is saying that people that have had COVID-19 need the vaccines. https://directorsblog.nih.gov/2021/02/23/is-one-dose-of-covid-19-vaccine-enough-after-covid-19-infection/ He cited that an NIH funded study in pre-print showed that people that had recovered from the wild infection showed a 10X or greater antibody response after their first vaccine dose than those who haven’t had COVID-19 after their first shot (reference below). His point of the article is to say that they may only need the first dose of the vaccine, but what he probably doesn’t even realize, is that he is essentially making the case that people who have had COVID-19 will have a robust antibody response when later exposed to the virus (in this case even just the spike protein from the vaccine). This basic virology. Antibodies may fall over time, but when presented with the virus (or vaccine), the Memory Cells are capable of kicking out high levels of antibodies once again. Is this simply ignorance or an agenda? I’m guessing ignorance, because he also said people that have had the infection need the vaccine to prevent “re-infection”. An opinion paper in USA Today February 28th, 2021 titled, COVID-19 cases are falling. This could be the beginning of the end of the pandemic, by Robert M. Kaplan, a faculty member at Stanford Medical School Clinical Excellence Research Center, a former associate director of the National Institutes of Health and a former chief science officer for the U.S. Agency for Health Care Research and Quality calls into question what Dr. Collins says. Dr. Kaplan stated that there have been only 57 documented cases of re-infection out of 113 million cases world-wide. I would hardly call this a reason to recommend all people that have infection with SARS-CoV-2 get an experimental vaccine with no long-term safety data. Many people claim that they know someone that has had it twice, but with the incredibly high false positive rates of the PCR test, the vast majority of those are just that…false alarms.

From Dr. Kaplan’s article:

“Once infected with SARS-CoV-2, natural immunity offers powerful protection. Although there are some cases of reinfection, they are extremely rare. Among 113 million confirmed COVID-19 cases worldwide, there are only 57 documented reinfections. The placebo group in the Johnson & Johnson vaccine study includes 2,030 people who had previously been infected. These individuals were better protected against clinical infection than those who got the vaccine.”

Once again back to Dr. Collins’ article:

“People who’ve recovered from COVID-19 also should definitely get vaccinated to maximize protection against possible re-infection. But, because they already have some natural immunity, would just one shot do the trick? Or, do they still need two? A small, NIH-supported study, published as a pre-print on medRxiv, offers some early data on this important question.” https://www.medrxiv.org/content/10.1101/2021.01.29.21250653v1.full.pdf (The study is titled: Robust spike antibody responses and increased reactogenicity in seropositive individuals after a single dose of SARS-CoV-2 mRNA vaccine). “These findings come from a research team led by Florian Krammer and Viviana Simon, Icahn School of Medicine at Mount Sinai, New York. The researchers reasoned that for folks whose bodies have already produced antibodies following a COVID-19 infection, the first shot might act similarly to the second one in someone who hadn’t had the virus before. In fact, there was some anecdotal evidence suggesting that previously infected people were experiencing stronger evidence of an active immune response (sore arm, fever, chills, fatigue) than never-infected individuals after getting their first shots.” “What did the antibodies show? To find out, the researchers enlisted the help of 109 people who’d received their first dose of mRNA vaccines made by either Pfizer or Moderna. They found that those who’d never been infected by SARS-CoV-2 developed antibodies at low levels within 9 to 12 days of receiving their first dose of vaccine.” “But in 41 people who tested positive for SARS-CoV-2 antibodies prior to getting the first shot, the immune response looked strikingly different. They generated high levels of antibodies within just a few days of getting the vaccine. Compared across different time intervals, previously infected people had immune responses 10 to 20 times that observed in uninfected people. Following their second vaccine dose, it was roughly the same story. Antibody levels in those with a prior infection were about 10 times greater than the others.” (Emphasis mine). (my comment: Imagine how the immune system in a post-infection person would perform if it was faced with the wild SARS-CoV-2 virus or any of its variants later on. Being able to recognize all of the proteins from the wild virus instead of just the spike protein from the vaccines will certainly provide greater recognition and response. (see the graph at the end of this segment) Now, that is exactly what the immune system should do Dr. Collins. And this phenomenon has been documented in numerous studies over the last many months. Even better, it is not just antibodies that remember the virus in those that have had COVID-19. It’s also the T-Cells and other immune players that mount an effective attack upon re-exposure to the virus. At any rate, thanks for referencing your NIH funded study Dr. Collins. It makes a makes a strong case against your unscientific positions. I know that wasn’t your intention though. For those interested in reading the rest of Dr. Kaplan’s opinion paper, he does a good job of discussing the estimated percentage of the population that have had the infection and relating it to being close to herd immunity even BEFORE the mass vaccine rollout. IMPORTANTLY, and against the narrative we will hear about the vaccines being responsible for the decline of infections, he says the following:

“Vaccines will be essential for ending the pandemic, but they don’t explain why cases are now quickly declining. Very few people had been inoculated when the decline started, and only more than 13% have received shots in the United States. Further, cases are dropping in countries that have initiated vaccination programs and those who have not started. Japan, where vaccinations only launched last week, had a 85% decline in new cases since Jan. 11. In Colombia, where vaccines are unavailable, new cases have fallen 78% since Jan. 20.”

Here is the link to Dr. Kaplan’s Opinion Paper: https://www.usatoday.com/story/opinion/2021/02/26/covid-19-vaccines-herd-immunity-pandemic-could-be-ending- column/6810858002/

Picture showing the various protein categories of the SARS-CoV-2 virus

*NOTE: The COVID shots only contain the “S” protein therefore providing the immune system with just a small fraction of all the viral proteins, whereas natural infection results in recognition of all viral proteins.

Two new studies provide more evidence of lasting immunity after infection with SARS-CoV-2

A May 26th 2021 article in the New York Times titled Immunity to the Coronavirus May Persist for Years, Scientists Find reinforces numerous studies from the last year that have demonstrated that immunity after infection with SARS-CoV-2 in durable and robust.

The article references two studies, one titled SARS-CoV-2 infection induces long-lived bone marrow plasma cells in humans, published May 24th, 2021, in the journal Nature.

The abstract

Long-lived bone marrow plasma cells (BMPCs) are a persistent and essential source of protective antibodies. Individuals who have recovered from COVID-19 have a substantially lower risk of reinfection with SARS-CoV-2. Nonetheless, it has been reported that levels of anti-SARS-CoV-2 serum antibodies decrease rapidly in the first few months after infection, raising concerns that long-lived BMPCs may not be generated and humoral immunity against SARS-CoV-2 may be short-lived. Here we show that in convalescent individuals who had experienced mild SARS-CoV-2 infections (n = 77), levels of serum anti-SARS-CoV-2 spike protein (S) antibodies declined rapidly in the first 4 months after infection and then more gradually over the following 7 months, remaining detectable at least 11 months after infection. Anti-S antibody titres correlated with the frequency of S-specific plasma cells in bone marrow aspirates from 18 individuals who had recovered from COVID-19 at 7 to 8 months after infection. S-specific BMPCs were not detected in aspirates from 11 healthy individuals with no history of SARS-CoV-2 infection. We show that S-binding BMPCs are quiescent, which suggests that they are part of a stable compartment. Consistently, circulating resting memory B cells directed against SARS-CoV-2 S were detected in the convalescent individuals. Overall, our results indicate that mild infection with SARS- CoV-2 induces robust antigen-specific, long-lived humoral immune memory in humans.

From the Discussion

Long-lived BMPCs provide the host with a persistent source of preformed protective antibodies and are therefore needed to maintain durable immune protection. However, the longevity of serum anti-S IgG antibodies is not the only determinant of how durable immune-mediated protection will be. Isotype-switched memory B cells can rapidly differentiate into antibody-secreting cells after re-exposure to a pathogen, offering a second line of defence34. Encouragingly, the frequency of S-binding circulating memory B cells at 7 months after infection was similar to that of B cells directed against contemporary influenza HA antigens. Overall, our data provide strong evidence that SARS-CoV-2 infection in humans robustly establishes the two arms of humoral immune memory: long-lived BMPCs and memory B cells. These findings provide an immunogenicity benchmark for SARS-CoV-2 vaccines and a foundation for assessing the durability of primary humoral immune responses that are induced in humans after viral infections. https://www.nature.com/articles/s41586-021-03647-4

The second study is titled, Vaccination boosts naturally enhanced neutralizing breadth to SARS-CoV-2 one year after infection. While as the title indicates, part of what the researchers were looking for is what vaccination would do to further boost antibody levels. While it did boost them (and that is no revelation because it is predictable and been shown previously), the exciting part to me is the following information they discovered about people that have had the SARS-CoV-2 infection and no vaccination.

From the study

Here we report on a cohort of 63 COVID-19-convalescent individuals assessed at 1.3, 6.2 and 12 months after infection, 41% of whom also received mRNA vaccines3,4. In the absence of vaccination antibody reactivity to the receptor binding domain (RBD) of SARS-CoV-2, neutralizing activity and the number of RBD-specific memory B cells remain relatively stable from 6 to 12 months.

Consistent with the longevity of bone marrow plasma cells, infection with SARS-CoV-2 leads to persistent serum anti-RBD antibodies, and corresponding neutralizing responses. Nearly 93% of the plasma neutralizing activity is retained between 6- and 12-months30,31.

However, neutralizing breadth increased between 1.3 and 12-months for all 15 pairs, even when neutralizing activity against the wild-type was unchanged or decreased (Fig. 5c and Supplementary Table 8). Only 1 of the 15 antibodies obtained after 1.3 months neutralized all the mutants tested (Fig. 5c). In contrast, 10 of the 15 antibodies obtained from the same clones after 12 months neutralized all variants tested with IC50s as low as 1 ng/ml against the triple mutant K417N/E484K/N501Y found in B.1.351 (Fig. 5c and Supplementary Table 8).

In conclusion, continued clonal evolution of anti-SARS-CoV-2 antibodies over 12 months favors increasing potency and breadth resulting in monoclonal antibodies with exceptional activity against a broad group of variants. https://www.biorxiv.org/content/10.1101/2021.05.07.443175v1

From the New York Times article

Important immune cells survive in the bone marrow of people who were infected with the virus or were inoculated against it, new research suggests. Immunity to the coronavirus lasts at least a year, possibly a lifetime, improving over time especially after vaccination, according to two new studies. The findings may help put to rest lingering fears that protection against the virus will be short-lived.

The studies may soothe fears that immunity to the virus is transient, as is the case with coronaviruses that cause common colds. But those viruses change significantly every few years, Dr. Hensley said. “The reason we get infected with common coronaviruses repetitively throughout life might have much more to do with variation of these viruses rather than immunity,” he said.

Upon first encountering a virus, B cells rapidly proliferate and produce antibodies in large amounts. Once the acute infection is resolved, a small number of the cells take up residence in the bone marrow, steadily pumping out modest levels of antibodies.

To look at memory B cells specific to the new coronavirus, researchers led by Ali Ellebedy of Washington University in St. Louis analyzed blood from 77 people at three-month intervals, starting about a month after their infection with the coronavirus. Only six of the 77 had been hospitalized for Covid-19; the rest had mild symptoms.

Antibody levels in these individuals dropped rapidly four months after infection and continued to decline slowly for months afterward — results that are in line with those from other studies. Some scientists have interpreted this decrease as a sign of waning immunity, but it is exactly what’s expected, other experts said. If blood contained high quantities of antibodies to every pathogen the body had ever encountered, it would quickly transform into a thick sludge.

Instead, blood levels of antibodies fall sharply following acute infection, while memory B cells remain quiescent in the bone marrow, ready to take action when needed.

Five of the participants in Dr. Ellebedy’s study donated bone marrow samples seven or eight months after they were initially infected and again four months later. He and his colleagues found that the number of memory B cells remained stable over that time.

The results are particularly noteworthy because it is difficult to get bone marrow samples, said Jennifer Gommerman, an immunologist at the University of Toronto who was not involved in the work. A landmark study in 2007 showed that antibodies in theory could survive decades, perhaps even well beyond the average life span, hinting at the long-term presence of memory B cells. But the new study offered a rare proof of their existence, Dr. Gommerman said.

Dr. Nussenzweig’s team looked at how memory B cells mature over time. The researchers analyzed blood from 63 people who had recovered from Covid-19 about a year earlier. The vast majority of the participants had mild symptoms, and 26 had also received at least one dose of either the Moderna or the Pfizer-BioNTech vaccine.

So-called neutralizing antibodies, needed to prevent reinfection with the virus, remained unchanged between six and 12 months, while related but less important antibodies slowly disappeared, the team found. As memory B cells continued to evolve, the antibodies they produced developed the ability to neutralize an even broader group of variants. This ongoing maturation may result from a small piece of the virus that is sequestered by the immune system — for target practice, so to speak.

“It kind of looks exactly like what we would hope a good memory B cell response would look like,” said Marion Pepper, an immunologist at the University of Washington in Seattle who was not involved in the new research.

End of excerpts https://www.nytimes.com/2021/05/26/health/coronavirus-immunity-vaccines.html

A study looking at two dozen other studies examining cross-reactivity to other coronavirus infections that provide protection against SARS-CoV-2

This study is a little more technical in nature and terminology.

Pre-existing reactivity and cross-reactivity with common cold corona and other viruses Several studies have detected responses to SARS-CoV-2 sequences in unexposed controls (Sette and Crotty, 2020b, Sette and Crotty, 2021). In some cases, these responses might correspond to infections associated with a lack of antibodies or to a transient antibody response (Sekine et al., 2020, Nelde et al., 2021). However, in other cases, these responses appear to be linked to preexisting memory responses, which, in some instances, have been mapped to the cross-reactive recognition of the SARS-CoV-2 sequences by T cells induced by endemic “common cold” coronaviruses (17) and potentially other viral species (Bacher et al., 2020, Le Bert et al., 2020b). This phenomenon has received considerable attention because of its potential to influence disease severity, vaccination outcomes, and because of its potential implications for herd immunity (Bacher et al., 2020, Sette and Crotty, 2020b, Sette and Crotty, 2021, Lipsitch et al., 2020, Sagar et al., 2021a).

Epitopes recognized in non-exposed individuals have been defined in 12 studies. In some cases, these SARS- CoV-2 epitopes had significant homology to common cold coronavirus sequences, with cross-reactivity demonstrated at the molecular level in several instances (Mateus et al., 2020). Other studies, as discussed in more detail below, have examined whether SARS-CoV-2-CoV- 2 specific T cells might cross-react with other more closely related viruses, such as SARS-CoV-2-CoV- 1 and the Middle East Respiratory Syndrome virus (MERS) (see also below). This issue is of relevance in the context of developing vaccines that can elicit T cell responses that broadly recognize coronaviruses of pandemic potential.

The topic of pre-existing immune responses and cross-reactivity with common cold coronaviruses was addressed by several studies that reported a range of findings. Schulien et al. detected cross-reactive T cells in longitudinal samples pre-and-post SARS-CoV-2 infection, and reported that these cells were expanded post in vitro restimulation (Schulien et al., 2021). Sekine et al. also detected widespread reactivity in non-exposed individuals using peptide pools (Sekine et al., 2020). Shomuradova et al. detected pre-existing T cell reactivity in unexposed donors using HLA-A2 tetramers, but at much lower levels compared to those seen in exposed individuals (Shomuradova et al., 2020). Nelde et al. tested the reactivity of non-exposed donors to epitopes identified in exposed individuals, and detected reactivity, albeit at lower levels, for several epitopes (Nelde et al., 2021). Keller et al. detected T cells with minimal cross reactivity with two homologous nucleocapsid peptides from NL63 and OC43 (Keller et al., 2020). Ferretti detected reactivity to OC43 and HKU1 sequences for 2 of 29 dominant epitopes, and no reactivity for NL63 and 229E (Ferretti et al., 2020). Rha et al. reported that the SARS-CoV-2 S 269-277 and S 1220-1228 epitopes had low homology to OC43, HKU1, 229E, and NL63, and that MHC class I multimer+ cells were not detected in unexposed subjects (Rha et al., 2021).

Prakash identified 24 epitopes, and of those, 11 recalled memory CD8+ T cells from unexposed healthy individuals (Prakash et al., 2020).

A potential explanation for the differences observed in the degree of cross-reactivity of epitope repertoires detected in infected and unexposed subjects is provided by the studies of Mateus et al. (Mateus et al., 2020) and Tarke et al (Tarke et al., 2021a). These studies demonstrated that, overall, 50% of the epitopes defined in unexposed donors were also recognized in SARS-CoV-2-infected subjects (Mateus et al., 2020, Tarke et al., 2021a), but also that the viral infection created a new repertoire of epitopes recognized only in infected subjects. Conversely, over 80% of the epitopes defined in SARS-CoV-2-infected subjects were not recognized in unexposed donors. This suggests that a pre-existing repertoire of cross-reactive T cells is present in unexposed donors, but that the SARS-CoV-2 infection generates a largely novel repertoire of T cells, in addition to the pre- existing one. Consistent with this view, the antigens dominantly recognized in exposed donors tend to only partially overlap with those dominant in non-exposed donors (Le Bert et al., 2020b).

The issue of how preexisting memory reactivity might influence immunity has been debated, and a firm conclusion has not been reached as yet (Lipsitch et al., 2020, Sette and Crotty, 2020a, Sette and Crotty, 2020b). While it is not expected that preexisting T cell reactivity might protect against infection, it is possible that preexisting SARS-CoV-2 cross-reactive T cells might modulate disease severity, as reported by a recent study (Sagar et al., 2021b), or might even modulate vaccine responsiveness, allowing for a faster or more vigorous response.

The study of protective versus detrimental T cell responses is important for determining the optimal T cell engagement strategies for vaccines. In addition to understanding the relationship between pre-existing immunity to human coronaviruses and host defense against SARS-CoV-2, it is relevant to also consider the contribution of COVID-19 vaccine-boosted cross-reactive immune responses to vaccine-induced protective immunity.

Infection with other viruses may have a neutralizing effect against SARS-CoV-2. Did public lockdown measures aid in the spread of SARS-CoV-2 and thus COVID- 19 disease?

A June 15th, 2021 study from the Journal of Experimental Medicine titled, Dynamic innate immune response determines susceptibility to SARS-CoV-2 infection and early replication kinetics, finds that other infections such as Rhinovirus (one of the viruses that cause the common cold), prior to being infected by SARS-CoV-2 has a protective effect against SARS-CoV-2 replication in its early stages. This would have profound effect on the ability of the virus to outpace the immune system during its early replication process. It would also make it more difficult for the person to transmit the virus on to others because the viral load would be significantly reduced. From the study- (Bold emphasis mine)

However, our experiments showed that prior RV infection protected against replication of SARS-CoV-2, that this protection was dependent upon ISG induction (ISG stands for Interferon Stimulated Genes, which activate the release of Interferon a powerful tool for activating immune response and reducing infection), and that a significant bystander IFN response was detected in cells throughout the epithelium for at least 5 d after RV infection, even after the RV itself was largely cleared (Figs. 5, 6, and S4). These results indicate that the protective effect of heterologous ISG induction throughout the epithelium by RV predominated over other effects, potently suppressing SARS-CoV-2 replication.

While host–pathogen interactions are often studied one at a time in experimental models, in the human upper respiratory tract, exposure to multiple microbes simultaneously or in series is a frequent occurrence and likely an important influence on innate immunity. The idea that viral interference could be shaping broad patterns of respiratory virus transmission has only recently begun to gain traction, in part due to epidemiological data suggesting interference among RNA respiratory viruses (Isaacs and Lindenmann, 1957; Greer et al., 2009; Linde et al., 2009; Casalegno et al., 2010; °Anestad and Nordbø, 2011; Schultz-Cherry, 2015; Karppinen et al., 2016; Nickbakhsh et al., 2019; Wu et al., 2020).

Heterologous ISG induction could be particularly important for host defense against a virus like SARS-CoV-2, since it would preempt mechanisms SARS-CoV-2 has in place to antagonize and delay IFN and ISG induction in response to its own replication.

The SARS-CoV-2 pandemic and the public health response have disrupted the status quo in many ways, including dramatically reducing the circulation of common respiratory viruses (Olsen et al., 2020; Jones, 2020; Cowling et al., 2020; Yeoh et al., 2020; Sullivan et al., 2020; Centers for Disease Control and Prevention, 2021b). This change has led to speculation that diminished population adaptive immunity will lead to a surge of infections when these viruses again recirculate, and thus far, early data from school reopenings indicate a likely robust resurgence of RV (Baker et al., 2020; Fong et al., 2021; Poole et al., 2020). Our findings suggest that heterologous innate immune responses could be a mitigating factor, since the model predicts an upper limit in the extent to which IFN-sensitive viruses can simultaneously or sequentially infect the same host (see model, Fig. 7 A). This would also potentially slow viral transmission in the population by reducing the number of susceptible hosts at any given time (Fig. 7 B). Importantly, we are proposing this model based on our data to highlight the importance of considering viral interference in epidemiological patterns that may emerge in the coming year, but we are not arguing that potential effects of heterologous innate immunity outweigh the proven benefits of public health measures for directly preventing SARS-CoV-2 transmission.

My comment: While it may have not been in the purview of this paper to argue that, I certainly would and could make a very good case for it.

Due to the nature of exponential growth, even a small change in the replication rate, as we observed with inhibition of ISG induction during low-MOI infection (Fig. 6, E–H), could have a profound impact on peak viral load. For example, if conditions allowed the viral doubling time to decrease by 2 h from 6 h to 4 h, this would lead to a 64-fold greater NP viral load after 72 h. NP viral load has been shown to correlate with viral transmission, an issue that has come into focus recently due to the emergence of SARS-CoV-2 variants with enhanced transmission (Cevik et al., 2021; He et al., 2020; Singanayagam et al., 2020; Centers for Disease Control and Prevention, 2021a). Our results suggest that viral mutations that enhance IFN/ISG antagonism would enable a faster doubling time and compel studying at this aspect of the biology as a possible mechanism for increased transmissibility in emerging viral variants.

In sum, our results demonstrate an important role for IFN mediated defenses in curtailing SARS-CoV-2 replication at the start of infection, including heterologous innate immune responses induced by prior RV infection. These results, and our findings in longitudinal patient samples, support the concept that airway innate immunity is dynamic, with innate immune defense rapidly changing in response to current and recent viral infections. Our findings also demonstrate that ISG-mediated defenses can profoundly curtail SARS-CoV-2 replication under certain conditions and compel further studies of the role of heterologous innate immunity in protecting against SARS-CoV-2 and other respiratory viruses.

End of excerpts

By reducing the number of susceptible hosts (as can be seen in the diagram above), it will slow the spread of infection in the community. This is just another powerful example of how the unprecedented draconian measures implemented to quarantine healthy people by locking down businesses, closing schools and encouraging stay at home orders once again had another negative effect on the outcome of the spread of the virus. This most certainly has contributed to the stresses we saw on our health care system, including severe cases and deaths.

The amazing duration of protection from the human immune system

What does Dr. Fauci know about long-term immunity compared to what he tells the public? Read this story to the end and you will find out what he has known for a very long time.

A study published in the journal Nature in 2008 revealed astounding evidence of decades of immunity after the 1918 Pandemic Spanish Flu!

In the study titled Researchers find long-lived immunity to 1918 pandemic virus, researchers took the blood from 32 people aged 91 to 101 that had survived the 1918 Spanish flu ninety years earlier and tested it to see if their immune system recognized and responses to cell proteins from that flu strain.

The findings appeared online Aug 17 in Nature. Study collaborators hail from several institutions: Vanderbilt University, Mount Sinai School of Medicine, University of Medicine and Dentistry of New Jersey (UMDNJ), the Centers for Disease Control and Prevention (CDC), and Scripps Research Institute.

The group collected blood samples from 32 pandemic survivors aged 91 to 101. The multipronged study had four components, to:

• Determine if the survivors still had antibodies to the virus • See if the B cells, the ones that produce the antibodies could be cultured and produce antibodies to a 1918 virus protein • Attempt fusing cells having the highest levels of activity with myeloma cells to create a hybrid cell line that secretes monoclonal antibodies • Evaluate if the antibodies could protect mice infected with the 1918 influenza virus

The people recruited for the study were 2 to 12 years old in 1918 and many recalled sick family members in their households, which suggests they were directly exposed to the virus, the authors report. The group found that 100% of the subjects had serum-neutralizing activity against the 1918 virus and 94% showed serologic reactivity to the 1918 hemagglutinin. The investigators generated B lymphoblastic cell lines from the peripheral blood mononuclear cells of eight subjects. Transformed cells from the blood of 7 of the 8 donors yielded secreting antibodies that bound the 1918 hemagglutinin

Author James E. Crowe, Jr, MD, professor of pediatrics and director of the Vanderbilt Program in Vaccine Sciences, said in a press release from Vanderbilt that the researchers were surprised by the findings. "The B cells have been waiting for at least 60 years if not 90 years for that flu to come around again," he said. "That's amazing, because it's the longest memory anyone's ever demonstrated. "From the B cells of three donors, the research group generated five monoclonal antibodies that not only strongly neutralized the 1918 virus, but also cross-reacted with proteins related to the 1930 swine flu virus. However, the antibodies did not react against more contemporary influenza strains. In the final arm of the study, the researchers infected mice with the reconstructed 1918 virus and the next day tested the five monoclonal antibodies at various doses to see if the therapy protected the animals. The mice receiving the lowest dose of the 1918 monoclonal antibody died, as did the ones receiving the control antibody. All given the highest antibody doses survived

They add that exposure to similar viruses circulating during first part of the 20th century probably bolstered the subjects' B cell function. Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, said recent studies have projected that immunity lasts several decades; the current study provides proof, the AP reported. "This is the mother of all immunological memory here," he told the AP.

Additional content added 08-01-21

Natural immunity appears to outperform vaccine immunity in the Memory Cells produced and residing in the bone marrow to release more antibodies with the next challenge from the virus

In report July 31st, 2021 from the British medical journal Lancet and titled Spike-antibody waning after second dose of BNT162b2 or ChAdOx1, the authors cite the following: “Our data suggest waning of S-antibody levels in infection-naive individuals over a 3–10-week period after a second dose of either ChAdOx1 or BNT162b2. These data are consistent with the decline in S-antibody and neutralising antibody levels observed after infection, although memory B-cell populations appear to be maintained.8,9 As such, the clinical implications of waning antibody levels post-vaccination are not yet clear, and it remains crucial to establish S-antibody thresholds associated with protection against clinical outcomes. End of excerpt

And a reference from the article points to a study supporting natural immunity published in Nature in March of 2021, that shows that these memory cells are well preserved, durable and provide robust action against future threat of infection. https://pubmed.ncbi.nlm.nih.gov/33461210/

NIH provides more evidence of long-term immunity after SARS-CoV-2 infection. Why doesn’t their policy follow the science published on their own web site?

An article published by the NIH on their Research Matters publication titled, Lasting immunity found after recovery from COVID-19, reported solid evidence of robust and lasting immunity 8 months after SARS-CoV-2 infection in 95% of the people tested. From the article After people recover from infection with a virus, the immune system retains a memory of it. Immune cells and proteins that circulate in the body can recognize and kill the pathogen if it’s encountered again, protecting against disease and reducing illness severity.

This long-term immune protection involves several components. Antibodies—proteins that circulate in the blood—recognize foreign substances like viruses and neutralize them. Different types of T cells help recognize and kill pathogens. B cells make new antibodies when the body needs them.

All of these immune-system components have been found in people who recover from SARS-CoV-2, the virus that causes COVID-19. But the details of this immune response and how long it lasts after infection have been unclear. Scattered reports of reinfection with SARS-CoV-2 have raised concerns that the immune response to the virus might not be durable. To better understand immune memory of SARS-CoV-2, researchers led by Drs. Daniela Weiskopf, Alessandro Sette, and Shane Crotty from the La Jolla Institute for Immunology analyzed immune cells and antibodies from almost 200 people who had been exposed to SARS-CoV-2 and recovered.

Time since infection ranged from six days after symptom onset to eight months later. More than 40 participants had been recovered for more than six months before the study began. About 50 people provided blood samples at more than one time after infection.

The research was funded in part by NIH’s National Institute of Allergy and Infectious Diseases (NIAID) and National Cancer Institute (NCI). Results were published on January 6, 2021, in Science.

The researchers found durable immune responses in the majority of people studied. Antibodies against the spike protein of SARS-CoV-2, which the virus uses to get inside cells, were found in 98% of participants one month after symptom onset. As seen in previous studies, the number of antibodies ranged widely between individuals. But, promisingly, their levels remained fairly stable over time, declining only modestly at 6 to 8 months after infection.

Virus-specific B cells increased over time. People had more memory B cells six months after symptom onset than at one month afterwards. Although the number of these cells appeared to reach a plateau after a few months, levels didn’t decline over the period studied.

Levels of T cells for the virus also remained high after infection. Six months after symptom onset, 92% of participants had CD4+ T cells that recognized the virus. These cells help coordinate the immune response. About half the participants had CD8+ T cells, which kill cells that are infected by the virus.

As with antibodies, the numbers of different immune cell types varied substantially between individuals. Neither gender nor differences in disease severity could account for this variability. However, 95% of the people had at least 3 out of 5 immune-system components that could recognize SARS-CoV-2 up to 8 months after infection.

“Several months ago, our studies showed that natural infection induced a strong response, and this study now shows that the responses last,” Weiskopf says. “We are hopeful that a similar pattern of responses lasting over time will also emerge for the vaccine-induced responses.” https://www.nih.gov/news-events/nih-research-matters/lasting-immunity-found-after-recovery-covid-19

This compilation of the science as it relates to lasting and robust immune response after infection with SARS-CoV-2 should be non-disputable. It is long time our public health officials follow the established science, rather than a dogma or ideology that is rooted in misinformation seemingly to induce public manipulation and control.

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The research and news on vaccines and infectious disease is coming at us fast and furious, especially now with the COVID-19 Pandemic. Even before that, media vaccine promotion followed predicable patterns, flu season hysteria, “dangerous” measles outbreaks, HPV vaccine promotions. But what is accurate and what is manufactured for our consumption, engineered to steer our thinking in a pharma driven compliant direction? Now with all things COVID-19, as the 24/7 media drives hysteria and fear mongering, a new push for mandated pharmaceutical intervention is on. The one thing history has proven and the COVID-19 crisis is no exception, is that expensive propitiatory patented new drugs and a new hastily developed experimental vaccine is not the answer. But the powers that be will do everything they can to employ those measures at the expense of our freedoms, our health and our economy. With the pharmaceutical industry accounting for 50-70% of advertising revenue to network, cable and social media outlets, it is no wonder that so much of the mainstream news is biased toward an agenda that pharma controls. That is why it is up to each individual to decipher fact from fiction and that is not always easy, especially when most consumers want their “facts” in short, quick sound bites. Well, I have a solution that makes that a possibility. I will search for and source “alternative” information that isn’t front page news (but should be), and bring it to you in concise, easy to digest bites in a monthly newsletter. And I will provide you with the data sources, so you can click and investigate them further if that is your desire! Then you can weigh the information against what is spoon fed to the masses and decide what you want to believe. Stay informed as this scenario plays out by subscribing to my monthly newsletter for just $6 per month. Subscribe here: https://www.wellnessdoc.com/science-and-news-monthly-newsletter/