Majority Are Already Immune Against SARS-CoV-2 by Dr. Joseph Mercola for Mercola
The more data becomes available about SARS-CoV-2, the more obvious it becomes that the response to this pandemic has been grossly overblown. Fatality statistics1,2,3,4,5,6,7 from multiple sources, calculated in a variety of ways, show the risk of dying from COVID-19 is lower than your risk of dying from conventional influenza, at least if you’re under the age of 60.
Overall, the data8,9 also show that the overall all-cause mortality has remained steady this year and doesn’t veer from the norm. In other words, COVID-19 has not killed off more of the population than would have died in any given year anyway.
Several studies also 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.
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Most Are Already Immune to SARS-CoV-2 Infection
Studies supporting the claim that widespread immunity against SARS-CoV-2 already exists include:
•Cell, June 202010,11 — This study found 70% of samples from patients who had recovered from mild cases of COVID-19 had resistance to SARS-CoV-2 on the T-cell level. Importantly, 40% to 60% of people who had not been exposed to SARS-CoV-2 also had resistance to the virus on the T-cell level.
According to the authors, this suggests there’s “cross-reactive T cell recognition between circulating ‘common cold’ coronaviruses and SARS-CoV-2.” In other words, if you’ve recovered from a common cold caused by a particular coronavirus, your humoral immune system may activate when you encounter SARS-CoV-2, thus rendering you resistant to COVID-19.
•Nature Immunology, September 202012 — This German study was initially posted on a preprint server in June 2020 under the title, “SARS-CoV-2 T-cell Epitopes Define Heterologous and COVID-19-Induced T-Cell Recognition.”13
It’s now published in the September 2020 issue of Nature Immunology with the slightly altered title, “SARS-CoV-2-Derived Peptides Define Heterologous and COVID-19-Induced T Cell Recognition.”14 Much like the Cell study above, this investigation also found that that:
“Cross-reactive SARS-CoV-2 peptides revealed pre-existing T cell responses in 81% of unexposed individuals and validated similarity with common cold coronaviruses, providing a functional basis for heterologous immunity in SARS-CoV-2 infection.”
In other words, even among those who were unexposed, 81% were resistant or immune to SARS-CoV-2 infection. The term “heterologous immunity” refers to immunity that develops against a given pathogen after you’ve been exposed to a nonidentical pathogen.
Typically, this occurs when viruses are sufficiently similar or from closely related species. In this case, SARS-CoV-2 appears to be sufficiently similar to coronaviruses that cause the common cold, so that if you’ve been exposed to any of those coronaviruses, your immune system is also able to combat SARS-CoV-2.
•The Lancet Microbe, September 202015,16 — This study found that rhinovirus infection, responsible for the common cold, largely prevented concurrent influenza infection by triggering the production of natural antiviral interferon.
The researchers speculate that the common cold virus could potentially help protect against SARS-CoV-2 infection as well. Interferon is part of your early immune response, and its protective effects last for at least five days, according to the researchers. Co-author Dr. Ellen Foxman told UPI:17
“Infection with the common cold virus protected cells from infection with a more dangerous virus, the influenza virus, and [this] occurred because the common cold activated the body’s general antiviral defenses.
This may explain why the flu season, in winter, generally occurs after the common cold season, in autumn, and why very few people have both viruses at the same time. Our results show that interactions between viruses can be an important driving force dictating how and when viruses spread through a population.
Since every virus is different, we still do not know how the common cold season will impact the spread of COVID-19, but we now know we should be looking out for these interactions.”
•Nature, July 202018,19,20 — Originally posted on a preprint server in May 2020,21 this Singaporean study was published in the July 2020 issue of Nature.22 Here, they found that common colds caused by the betacoronaviruses OC43 and HKU1 might make you more resistant to SARS-CoV-2 infection, and that the resulting immunity could potentially be long-lasting.
Patients who recovered from SARS infection back in 2003 still had T cell reactivity to the N protein of SARS-CoV now, 17 years later. These patients also had strong cross-reactivity to the N protein of SARS-CoV-2.
The authors suggest that if you’ve beaten a common cold caused by a OC43 or HKU1 betacoronavirus in the past, you may have a 50/50 chance of having defensive T-cells that can recognize and help defend against SARS-CoV-2. According to the authors:
“These findings demonstrate that virus-specific T cells induced by infection with betacoronaviruses are long-lasting, supporting the notion that patients with COVID-19 will develop long-term T cell immunity.
Our findings also raise the possibility that long-lasting T cells generated after infection with related viruses may be able to protect against, or modify the pathology caused by, infection with SARS-CoV-2.”
•Cell August 202023,24 — This Swedish study, initially posted on a preprint server in June 202025 and now published in the October 2020 issue of the journal Cell,26 found that SARS-CoV-2-specific memory T cells likely provide long-term immune protection against COVID-19. According to the authors:27
“Acute-phase SARS-CoV-2-specific T cells displayed a highly activated cytotoxic phenotype that correlated with various clinical markers of disease severity, whereas convalescent-phase SARS-CoV-2-specific T cells were polyfunctional and displayed a stem-like memory phenotype.
Importantly, SARS-CoV-2-specific T cells were detectable in antibody-seronegative exposed family members and convalescent individuals with a history of asymptomatic and mild COVID-19.
Our collective dataset shows that SARS-CoV-2 elicits broadly directed and functionally replete memory T cell responses, suggesting that natural exposure or infection may prevent recurrent episodes of severe COVID-19.”
