Search

SARS-CoV-2 Antibody Update

James P.M. Odell, OMD, ND, L.Ac.

A mainstream news narrative that we are starting to hear more of is that even though natural immunity after recovery from SARS-CoV-2 infection appears to be quite good, “we don’t know how long it’ll last.” This is rather disingenuous, seeing how natural immunity from specific organisms is typically lifelong, and studies have shown natural immunity against SARS-CoV-2 is longer lasting than vaccine-induced immunity. This article will discuss aspects of the immune system relative to natural and artificial (vaccine) immunity and highlight the importance of natural immunity.

Overview of the Immune System

Since the appearance of life on Earth, natural immunity has been developing in all living beings in response to microbial entities (and all this without vaccines). The immune system can be divided into two main subsystems, the innate/general resistance system, and the adaptive system. Both the innate system and the adaptive system continually interact with each other to provide an effective immune response.

Innate Immunity

Innate immunity precedes adaptive immunity and has allowed us to recognize foreign pathogens, eliminate them and maintain an immune memory. The innate immune system, or general resistance, includes a variety of protective measures which are continually functioning and provide a first line of defense against pathogenic agents. However, these responses are not specific to a particular pathogenic agent. Instead, the innate immune cells are specific for conserved molecular patterns found on all microorganisms. This prevents the innate immune system from inadvertently recognizing host cells and attacking them. However, this prevents the innate immune responses from improving their reactions with repeated exposure to the same pathogenic agent. In other words, the innate immune system does not have memory.

The protective defenses of the innate immune system begin with anatomic barriers such as intact skin and mucous membranes which prevent the entrance of many microorganisms and toxic agents. The skin also has an acidic environment of pH 3-5 which retards the growth of microorganisms. In addition, the normal microorganisms or flora (the microbiome), which inhabit the skin and mucous membranes compete with other microorganisms for nutrients and attachment sites. Further, the mucus and cilia aids the mucous membranes in trapping microorganisms and propelling them out of the body.1

Next, the innate immune system includes physiologic barriers such as normal body temperature, fever, gastric acidity, lysozyme, interferon, and collectins. The normal body temperature range inhibits a variety of microorganisms, and the development of fever can further inhibit many of these pathogenic organisms. The gastric acidity of the stomach is also quite effective in eliminating many ingested microorganisms. Lysozyme, which is a hydrolytic enzyme found in tears and mucous secretions, can cleave the peptidoglycan layer of the bacterial cell wall thus lysing the microorganism. Interferon(s), which include(s) a group of proteins that are produced by virally infected cells, can bind to noninfected cells and produce a generalized antiviral state. Interferon is a chemical that cells emit when infected by something foreign. The chemical switches on defenses in all the surrounding cells and consequently protects the surrounding cells from viral attack - a bit like a force field of protection. Without interferon, cells would be much more susceptible to almost every disease, bacteria, and virus that exists. Collectins are surfactant proteins that are present in serum, lung secretions, and mucosal surfaces. They can directly kill certain pathogenic microorganisms by disrupting their lipid membranes or indirectly by clumping microorganisms to enhance their susceptibility to phagocytosis.2

The innate immune system is part of, and inter-dependent on the body’s internal terrain – pH, level of extracellular toxicity, etc. Thus, extracellular toxicity and substances that suppress innate immunity can greatly compromise the body’s overall immune system.

White cells called mononuclear phagocytes and granulocytic cells, are important to the innate response and help link the innate immune response to the adaptive immune response. Mononuclear phagocytes include monocytes that circulate in the blood and macrophages which are in the tissues. Monocytes and macrophages are highly important in antigen presentation, phagocytosis, cytokine production, and antimicrobial and cytotoxic activities.3

When strong and not suppressed, the innate system can eradicate the pathogenic agent without further assistance from the adaptive system; or the innate system may stimulate the adaptive immune system to become involved in eradicating the pathogenic agent.

The complement pathways are also a part of the defensive measures of the innate immune system. This is rather complex, but briefly speaking, there are three complement pathways:

  1. The classical pathway is triggered when IgM antibodies or certain IgG antibody subclasses bind surface markers/antigens on microorganisms.

  2. The alternative or properdin pathway is triggered by the deposition of complement protein, C3b, onto microbial surfaces and does not require antibodies for activation.

  3. The third pathway, the lectin pathway, is triggered by the attachment of plasma mannose-binding lectin to microbes and does not require antibodies for activation.

These three pathways merge into a common pathway which leads to the formation of the membrane attack complex that can form pores in the membrane of targeted cells. The complement pathways are also integral in the opsonization (or increased susceptibility) of particulate antigens to phagocytosis and in triggering a localized inflammatory response.4


Adaptive Immunity

In contrast to the innate immune system, the actions of the adaptive immune system are specific to the pathogenic agent. This response will take longer to occur than the innate response. However, the adaptive immune system has memory which means that the adaptive immune system will respond more rapidly to that particular pathogen with each successive exposure.

The adaptive immune response is composed of the B–cells/antibodies and T-cells. These are the two arms of the adaptive immune system. The B–cells and antibodies compose humoral immunity or antibody-mediated immunity; and the T-cells compose cell-mediated immunity. (As a note, natural killer cells are also from the lymphocyte lineage like B–cells and T-cells; however, natural killer cells are only involved in innate immune responses.) An important part of adaptive immunity is cell-mediated immunity, which functions primarily against intracellular pathogens. T-cells mature in the thymus and are then released into the bloodstream. There are two main types of T-cells, CD4 cells and CD8 cells.

Both the innate and adaptive immune subsystems are necessary to provide an effective immune response whether to an actual pathogenic agent or a vaccine. Active immunization occurs with the exposure of an unimmunized individual to a pathogenic agent. The immune system of this individual then begins the process of developing immunity to this agent. Active immunization can occur either naturally or artificially. In immunology, it has long been observed that natural immunity is stronger, more permanent, and robust than artificial immunity from vaccines.

Natural Immunity as it Pertains to SARS-CoV-2 Infection

Below is a chronological sampling of scientific publications that have investigated natural immunity as it pertains to SARS-CoV-2 infection. There is rigorous ongoing research in this area, all pointing to the robust and long-lasting integrity of natural immunity.

  • A May 2020 report in the journal Immunity confirmed that SARS-CoV-2-specific neutralizing antibodies are detected in COVID-19 convalescent subjects, as well as cellular immune responses. Here, they found that neutralizing antibody titers do correlate with the number of virus-specific T cells. They further concluded, “In our study, production of S-RBD-specific antibodies were readily detected in recovered patients. Moreover, we observed virus-neutralization activities in these recovered patients. Not surprisingly, a significant correlation between neutralizing antibody titers and AUC of anti-S-RBD IgG, but not anti-NP IgG, was observed. Anti-S-RBD IgG might be useful in analyzing serum neutralization capabilities in COVID-19 patients. Our data are consistent with the work from other investigators (Zhou et al., 2020), in keeping with the role of humoral immunity in a blockade of receptor binding during viral entry in host cells.”5

  • Science Immunology October 2020 found that “RBD-targeted antibodies are excellent markers of previous and recent infection, that differential isotype measurements can help distinguish between recent and older infections, and that those IgG responses persist over the first few months after infection and are highly correlated with neutralizing antibodies.” They also concluded, “These findings also add to emerging evidence on the persistence and decay of antibody responses following SARS-CoV-2 infection. IgM and IgA responses to RBD were short-lived and most individuals seroreverted within two and a half months after the onset of illness. However, IgG antibodies persisted at detectable levels in patients beyond 90 days after symptom onset, and seroreversion was only observed in a small percentage of individuals.”6

  • The BMJ January 2021 concluded that “Of 11,000 healthcare workers who had proved evidence of infection during the first wave of the pandemic in the UK between March and April 2020, none had symptomatic reinfection in the second wave of the virus between October and November 2020. As a result, the researchers felt confident that immunity to reinfection lasts at least six months in the case of the novel coronavirus, with further studies required to understand much more.”7

  • Science February 2021 reported that “Substantial immune memory is generated after COVID-19, involving all four major types of immune memory [antibodies, memory B cells, memory CD8+ T cells, and memory CD4+ T cells]. About 95% of subjects retained immune memory at ~6 months after infection. Circulating antibody titers were not predictive of T cell memory. Thus, simple serological tests for SARS-CoV-2 antibodies do not reflect the richness and durability of immune memory to SARS-CoV-2.” A 2,800-person study found no symptomatic reinfections over a ~118-day window, and a 1,246-person study observed no symptomatic reinfections over 6 months.”8

  • A February 2021 study posted on the prepublication server medRxiv concluded that “Reinfection is rare. Natural infection appears to elicit strong protection against reinfection with an efficacy ~95% for at least seven months.”9

  • An April 2021 Israel study posted on medRxiv reported “the overall estimated level of protection from prior SARS-CoV-2 infection for documented infection is 94.8%; hospitalization 94.1%; and severe illness 96·4%. Our results question the need to vaccinate previously-infected individuals.”10

  • Another April 2021 study posted on the preprint server BioRxiv concluded that “following a typical case of mild COVID-19, SARS-CoV-2-specific CD8+ T cells not only persist but continuously differentiate in a coordinated fashion well into convalescence, into a state characteristic of long-lived, self-renewing memory.”11

  • A May 2021 Nature article found SARS-CoV-2 infection induces long-lived bone marrow plasma cells, which are a crucial source of protective antibodies. Even after a mild infection, anti-SARS-CoV-2 spike protein antibodies were detectable beyond 11 months post-infection. They conclude, “Overall, our results indicate that mild infection with SARS-CoV-2 induces robust antigen-specific, long-lived humoral immune memory in humans.”12

  • A May 2021 study in E Clinical Medicine found “antibody detection is possible for almost a year post-natural infection of COVID-19.” According to the authors, “Based on current evidence, we hypothesize that antibodies to both S and N-proteins after natural infection may persist for longer than previously thought, thereby providing evidence of sustainability that may influence post-pandemic planning.”13

  • A June 2021 Nature article points out that “Wang et al. show that, between 6 and 12 months after infection, the concentration of neutralizing antibodies remains unchanged. That the acute immune reaction extends even beyond six months is suggested by the authors’ analysis of SARS-CoV-2-specific memory B cells in the blood of the convalescent individuals over the course of the year. These memory B cells continuously enhance the reactivity of their SARS-CoV-2-specific antibodies through a process known as somatic hypermutation. The good news is that the evidence thus far predicts that infection with SARS-CoV-2 induces long-term immunity in most individuals.”14

  • Another June Nature paper concluded that “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.” According to the authors, the data suggest “immunity in convalescent individuals will be very long-lasting.”15

  • Lastly, Cure-Hub data confirm that “while COVID shots can generate higher antibody levels than natural infection, this does not mean vaccine-induced immunity is more protective. Importantly, natural immunity confers much wider protection as your body recognizes all five proteins of the virus and not just one. With the COVID vaccine, your body only recognizes one of these proteins, the spike protein. In addition, vaccination of convalescent subjects could be risky: more systemic adverse events are observed in convalescent subjects than in naïve subjects after the first dose of vaccine. Vaccination may decrease the ability to respond to future variants. It could also have a non-specific effect of remodeling the innate immune response by decreasing the potential response to other viruses or cancers and by modifying the course of inflammatory and autoimmune diseases.”16

Mucosal Immunity

The role of mucosal immunity, which is stimulated by natural infection and not by intramuscular vaccination, is a neglected but critical aspect of the overall immunity of SARS COV-2 infection. A 2020 study in Frontiers in Immunity reported, "Almost all studies of the immune response in COVID-19 have focused exclusively on serum antibodies and systemic cell-mediated immunity, including innate responses. Secretory IgA (SIgA) antibodies are known to be effective against various pathogens, including viruses, by such mechanisms as neutralization, inhibition of adherence to and invasion of epithelial cells, agglutination, and facilitation of removal in the mucus stream. Mucosal immunity and secretory and circulating IgA antibodies play an important role in COVID-19, and it is important to elucidate this to understand in particular the asymptomatic and mild states of infection, which appear to represent the majority of cases."17

This research highlights the importance of a balanced intestinal microbiome. Thus, dietary factors and probiotics that support the intestinal mucosa and its immunological function are critically important in both the prevention and treatment of SARS-CoV-2, as well as other pathogenic organisms.

Natural Immunity Superior to Artificial Immunity

One reason natural immunity is superior to vaccine-induced immunity is that the COVID-19 virus contains several different proteins. Of the 29 SARS-CoV-2 proteins, four make up the virus’s actual structure, including the S protein. The COVID “vaccine” induces antibodies against just one of those proteins, the spike protein, and elicits no T cell immunity. When you are infected with the whole virus, you develop antibodies against all parts of the virus, plus memory T cells. This also means natural immunity offers better protection against variants, as it recognizes several parts of the virus. If there are significant alterations to the spike protein, as with the ‘Delta variant,’ vaccine-induced immunity can be evaded. Not so with natural immunity, as the other proteins are still recognized and attacked.

Thus, natural immunity to Covid-19 (i.e., obtained after natural infection with the virus) is certainly robust and durable. Work on post- “vaccination” immunity is mainly concerned with so-called "neutralizing" antibodies in vitro. The levels of these antibodies are not an accurate correlate of protection because studies often find initially higher levels of antibodies after vaccination than after infection. However, because these artificially induced antibodies often quickly diminish, reinfections are much more frequent in inoculated Covid patients than in convalescents. Thus, we see “breakthrough infections.” Protection against Covid-19 rather depends on immune memory (due to memory T and B cells that persist long after infection) and are demonstrated to be of better quality than that conferred by “vaccines.” It is normal to observe an initial drop in circulating antibody levels after infection, as happens with all infections, otherwise, the blood would be thickened by all the antibodies that accumulate over a lifetime. At the same time, the immune memory is built and refined.

Additionally, inoculation of convalescent subjects is risky, very risky. More systemic adverse events are observed in convalescent subjects than in subjects after the first dose of “vaccine.” Not to mention the hundreds of thousands worldwide (if not millions) that have suffered severe vaccine reactions and the tens of thousands of deaths reported post-inoculation.

These inoculations can also decrease the ability to respond to future variants. It could have a non-specific effect of remodeling the innate immune response by decreasing the potential response to other viruses or cancers and by adversely modifying the course of inflammatory and autoimmune diseases. Many cancers and recurrence of autoimmune diseases are now being reported post-inoculation.


SARS-CoV-2 Inoculation Reduces Innate Immune Cell Response

Even more concerning, we hear arguments in scientific circles that vaccinal antibodies can suppress or subvert components of the innate immune system and this can leave the vaccinated immunologically weakened. This is particularly important for children, as they depend on their innate immunity and specifically innate antibodies to protect against a broad array of pathogens. Children and young people have quite a strong innate immune response and this naturally protects them from pathogenic viruses. If exposed to the COVID virus this generally will, in turn, boost their natural innate immunity. Conversely, in elderly persons, innate immunity wanes with age and this non-specific innate immunity gets replaced by antigen-specific immunity. Thus, the elderly are generally less protected and more susceptible to infections. This observation is certainly not new, as the elderly have always been sheltered during cold and flu season.

This study by Föhse et al. has shown that BNT162b2 mRNA (Pfizer) vaccine against SARS-CoV-2 reprograms both adaptive and innate immune responses. These results are very troubling as it reveals the vaccine is driving complex functional reprogramming of innate immune responses. This results in unknown long-term immune system dysregulation and derangement. Particularly, the dysregulation of the innate immune system in children could leave them defenseless to the COVID virus as well as other viruses (latent).18

These researchers demonstrated a decreased Interferon-gamma (IFN-γ) production following vaccination. IFN-γ is a key player in driving cellular immunity and is capable of orchestrating numerous protective functions to heighten immune responses in infections and cancers. It can exhibit its immunomodulatory effects by enhancing antigen processing and presentation, increasing leukocyte trafficking, inducing an anti-viral state, boosting the anti-microbial functions, and affecting cellular proliferation and apoptosis.

Thus, the concerning interest is the plummeting immune response among inoculated participants. This infers those fatalities from cancer and common infections such as winter colds and flu are set to skyrocket over the next 6 months. This is because when vaccine titers drop this opens the risk of developing antibody-dependent enhancement (ADE), also called pathogenic priming. ADE occurs when the antibodies generated during an immune response to a vaccine recognize and bind to a pathogen (virus), but they are unable to prevent infection. Instead, these antibodies act like a “Trojan horse”, allowing the pathogen to enter the organs and cells and severely exacerbating the immune response. This causes a “cytokine storm” of systemic inflammation. Thus, what is coming is a potential global wave of deaths from autoimmune diseases, cancer, and from common infections due to ADE that will likely overwhelm hospitals in 2022.


Keeping the Immunity Vital

No one food or supplement can prevent illness, but a good nutritional variety, including vitamin C, D3, zinc, quercetin, and probiotics regularly, may offer protection from seasonal illnesses. The type and dosage of supplements should be tailored to the individual’s unique biochemistry and need. Therefore, consult a health professional before embarking on any new supplemental regime. Stress, being out of shape, being overweight or obese, undernourishment, and nutritional deficiencies all can impair immune system responses. Lastly, adequate sleep is essential for immune health and recovery from illness.

Conclusion

As we distinguish the different roles of the innate immune system, versus vaccine-induced immunity (by hijacking our adaptive immune system), it is critical that we understand that these ‘vaccines’ offer absolutely no protection against infection. It is the innate immune system that protects us from outside invaders. The vaccine is engineered for the inside of the cell to create antibodies once exposed. Meanwhile, these mechanisms shift the balance of the immune system to leave our primary defense, the innate immune system, more vulnerable. Numerous studies have now demonstrated that natural immunity confers longer-lasting and stronger protection against infection, symptomatic disease, and hospitalization caused by the SARS-CoV-2, compared to the current inoculations.


References

  1. Goldsby, R. A., T. J. Kindt, B. A. Osborne, and J. Kuby. "Leukocyte migration and inflammation." Immunology, 5th ed. WH Freeman & Co., New York, NY (2003): 338-360.

  2. Hartshorn, Kevan L., Mitchell R. White, and Erika C. Crouch. "Contributions of the N-and C-terminal domains of surfactant protein d to the binding, aggregation, and phagocytic uptake of bacteria." Infection and immunity 70, no. 11 (2002): 6129-6139. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC130308/

  3. The Merck Manuals Online Medical Library. 2008. Components of the Immune System. [Last cited on 2009 Nov 26]. Available from: http://www.merck.com/mmpe/sec13/ch163/ch163b.html .

  4. The Merck Manuals Online Medical Library. 2008. Complement System. [Last cited on 2009 Nov 22]. Available from: http://www.merck.com/mmpe/sec13/ch163/ch163d.html .

  5. Ni, Ling, Fang Ye, Meng-Li Cheng, Yu Feng, Yong-Qiang Deng, Hui Zhao, Peng Wei et al. "Detection of SARS-CoV-2-specific humoral and cellular immunity in COVID-19 convalescent individuals." Immunity 52, no. 6 (2020): 971-977. https://www.sciencedirect.com/science/article/pii/S1074761320301813

  6. Iyer, Anita S., Forrest K. Jones, Ariana Nodoushani, Meagan Kelly, Margaret Becker, Damien Slater, Rachel Mills et al. "Persistence and decay of human antibody responses to the receptor binding domain of SARS-CoV-2 spike protein in COVID-19 patients." Science immunology 5, no. 52 (2020). https://www.science.org/doi/10.1126/sciimmunol.abe0367

  7. Stokel-Walker, Chris. "What we know about covid-19 reinfection so far." bmj 372 (2021). https://www.bmj.com/content/372/bmj.n99

  8. Dan, Jennifer M., Jose Mateus, Yu Kato, Kathryn M. Hastie, Esther Dawen Yu, Caterina E. Faliti, Alba Grifoni et al. "Immunological memory to SARS-CoV-2 assessed for up to 8 months after infection." Science 371, no. 6529 (2021). https://www.science.org/doi/10.1126/science.abf4063

  9. Abu-Raddad, Laith J., Hiam Chemaitelly, Peter Coyle, Joel A. Malek, Ayeda A. Ahmed, Yasmin A. Mohamoud, Shameem Younuskunju et al. "SARS-CoV-2 reinfection in a cohort of 43,000 antibody-positive individuals followed for up to 35 weeks." medRxiv (2021). https://www.medrxiv.org/content/medrxiv/early/2021/02/08/2021.01.15.21249731.full.pdf

  10. Goldberg, Yair, Micha Mandel, Yonatan Woodbridge, Ronen Fluss, Ilya Novikov, Rami Yaari, Arnona Ziv, Laurence Freedman, and Amit Huppert. "Protection of previous SARS-CoV-2 infection is similar to that of BNT162b2 vaccine protection: A three-month nationwide experience from Israel." medRxiv (2021). https://www.medrxiv.org/content/medrxiv/early/2021/04/24/2021.04.20.21255670.full.pdf

  11. Ma, Tongcui, Heeju Ryu, Matthew McGregor, Benjamin Babcock, Jason Neidleman, Guorui Xie, Ashley F. George et al. "Protracted yet coordinated differentiation of long-lived SARS-CoV-2-specific CD8+ T cells during COVID-19 convalescence." bioRxiv (2021). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8095211/

  12. Turner, Jackson S., Wooseob Kim, Elizaveta Kalaidina, Charles W. Goss, Adriana M. Rauseo, Aaron J. Schmitz, Lena Hansen et al. "SARS-CoV-2 infection induces long-lived bone marrow plasma cells in humans." Nature (2021): 1-5. https://www.nature.com/articles/s41586-021-03647-4

  13. Alfego, David, Adam Sullivan, Brian Poirier, Jonathan Williams, Ajay Grover, Laura Gillim, Dorothy Adcock, and Stanley Letovsky. "A population-based analysis of the longevity of SARS-CoV-2 antibody seropositivity in the United States." EClinicalMedicine 36 (2021): 100902. https://www.sciencedirect.com/science/article/pii/S2589537021001826

  14. Radbruch, Andreas, and Hyun-Dong Chang. "A long-term perspective on immunity to COVID." Nature (2021). https://www.nature.com/articles/d41586-021-01557-z?fbclid=IwAR3GSa3K_HkEx7Fto0ZF0jiZoYROnHvENCE05iCbDR77Z3CuGQlD6bO-dQg

  15. Wang, Zijun, Frauke Muecksch, Dennis Schaefer-Babajew, Shlomo Finkin, Charlotte Viant, Christian Gaebler, Hans-Heinrich Hoffmann et al. "Naturally enhanced neutralizing breadth against SARS-CoV-2 one year after infection." Nature 595, no. 7867 (2021): 426-431. https://www.nature.com/articles/s41586-021-03696-9

  16. Banoun, Helene. "Covid-19: Natural immunity versus vaccine immunity." Qeios (2021). https://www.qeios.com/read/DP264J

  17. Russell, Michael W., Zina Moldoveanu, Pearay L. Ogra, and Jiri Mestecky. "Mucosal immunity in COVID-19: a neglected but critical aspect of SARS-CoV-2 infection." Frontiers in Immunology 11 (2020): 3221. https://internal-journal.frontiersin.org/articles/10.3389/fimmu.2020.611337/full

  18. Föhse, F. Konstantin, Büsranur Geckin, Gijs J. Overheul, Josephine van de Maat, Gizem Kilic, Ozlem Bulut, Helga Dijkstra et al. "The BNT162b2 mRNA vaccine against SARS-CoV-2 reprograms both adaptive and innate immune responses." (2021). https://www.medrxiv.org/content/10.1101/2021.05.03.21256520v1.full