Herd Immunity to Covid-19 May Be Closer than Expected Based on New Discoveries


The SARS-CoV-2 is in many ways unlike any other coronavirus, but in some fortunate ways it shares some common features. The fact that it appears to be a coronavirus manipulated in a lab via “gain of function” research may be the key reason for some of the unusual features. Noted virologist Birger Sørensen and his colleagues provide convincing evidence supporting a laboratory origin of this pandemic in an article that you can read by clicking here. Sørensen calls the virus the perfect human pathogen. His conclusions have not been reported by the media and he has had difficulty publishing his findings in a scientific journal. They are politically controversial, but they are scientifically valid, detailed and accurate, nonetheless. Sørensen is not alone as there are other technical articles that are even more incriminating.

In this newsletter, I will share new data that explains some of the odd findings regarding how this virus interacts with our immune system. For example, why do so many people who have been infected with the virus have their antibodies to SARS-CoV-2 completely disappear a few months after the infection. I am not aware of any other infectious organisms that produces an infection and then the host’s immune system “forgets” how to make antibodies against it.

So, why would the immune system react this way? Why would immunity to the virus just seem to disappear? The answer may be that immunity did not vanish; it may simply mean that antibodies are just not that important in fighting against this particular virus as other aspects of immunity. The immune system has a lesser known method in developing specific and retained immunity to a virus. This method is called cell-mediated immunity and it is expressed by white blood cells known as T cells. Two incredible new studies point to the key aspect of immunity that T cells play in determining susceptibility and severity of COVID-19 as well as establishing immunity against SARS-CoV-2.

This new data, along with prior evidence, indicates that approximately 40-60% of healthy people already show at least a partial immune response to SARS-CoV-2 because of prior exposure to types of coronavirus that cause the common cold. If these findings prove to be accurate, then we may be much closer to herd immunity than expected and, if this virus runs its course, a vaccine may not be necessary. The good news there is that SARS-CoV-2 appears to be mutating to a more infectious, but less lethal form. That also bodes well for herd immunity as well as a lower mortality rate. Please read on….

Background Data:

The immune system is composed of many interrelated parts and systems. Nonspecific immunity involves the first line of defense from the immune system to infection. This includes proper barrier function, certain immune cells, and general defense mechanisms. Developing an immune response to defend against a specific organism is produced through “adaptive immunity.” It is composed of two divisions:

  • Antibody-mediated immune responses utilizing antibodies, which are special proteins produced by a type of white blood cell known as B cells. Antibodies bind to antigens (proteins on the virus or other organism) that ultimately trigger its destruction.
  • Cell-mediated immune responses enlist white blood cells known as T cells to directly attack viruses and/or infected cells. Cell-mediated immune responses do not involve antibodies.

 Cell-mediated immunity has taken a backseat to antibody-mediated mechanisms because of the focus on vaccines that produce primarily an antibody response, but cell-mediated immunity appears to be the more important adaptive immune response against SARS-CoV-2.

 Optimal cell-mediated immunity depends upon adequate nutrition and the proper functioning of the thymus gland. This gland lies in the upper chest in a bib-like fashion and is the master control center for cell-mediated immunity through its effect on T cells. These cells are produced as immature cells in bone marrow, but then migrate and mature in the thymus. The thymus gland also secretes various substances that control T cell activity.


There are several different forms of T cells. Cytotoxic T cells are able to directly kill virus-infected cells as well as cancer cells. Helper T cells signal other white blood cells to bring them into the fight. Regulatory or suppressor T cells are important in helping the immune system know the difference between attacking the body’s own tissue in an autoimmune response versus attacking an infectious organism or cancer cell. Memory T cells have been trained to recognize specific antigens to trigger a faster and stronger immune response after encountering the same antigen. Memory T cells play a central role in protecting against reinfection.

New Data:

In a study published on June 29 in bioRxiv,1 researchers systematically mapped the response of T cells specific to SARS-CoV-2 in a large group of individuals including:

  • Individuals who had not been exposed to the virus.
  • Individuals who were exposed to other family members with COVID-19.
  • Individuals with acute COVID-19.
  • Individuals who had fully recovered from COVID-19.

Let’s start with the people with acute COVID-19. As expected, in the acute phase of infection, SARS-CoV-2-specific T cells were highly activated to exert a cytotoxic (cell-killing) effect. In those that had recovered from COVID-19 the T cells displayed multiple functions against SARS-CoV-2. In individuals with a history of asymptomatic or mild COVID-19 along with positive antibody tests SARS-CoV-2-specific T cells as well as memory T cells were identified. Again, these results were expected. Now, here is where things get most interesting. In family members exposed to COVID-19 who had no detectable antibody response to SARS-CoV-2, the surprise finding was that SARS-CoV-2-specific T cells and memory T cells were detectable These results indicate that natural exposure to the virus, even if no infection occurs, can produce a robust memory T cell response akin to those observed in the context of successful vaccines. The researchers concluded that “natural exposure or infection may prevent recurrent episodes of severe COVID-19” even in people who have NO detectable antibodies to the virus.

The second study, published in the prestigious journal Nature on July 15, 2020, researchers first looked at the T cells in COVID-19 recovered patients. Results showed that the recovered patients possessed long-lasting memory T cells that are reactive to various SARS-CoV-2 antigens some of which are 100% identical to antigenic proteins found on other SARS-CoV-1. They then decided to look for and found the presence of memory T cells responsive to these proteins in subjects who had recovered from SARS-CoV-1 up to 11 years after they were infected. This indicates that subjects who developed SARS-CoV-1 infection may be immune to SARS-CoV-2.

They also looked at SARS-CoV-2 specific T cells in individuals with no history of SARS, COVID-19 or contact with SARS/COVID-19 patients. Surprisingly, they also frequently found these individuals had SARS-CoV-2 responsive T cells. These T cells in uninfected subjects exhibited a different pattern of response that showed recognition of protein fragments that are common to both SARS-CoV-2 viruses and “common cold” versions of human coronaviruses. The researchers concluded that prior infection with other coronaviruses, including those that cause the common cold, can produce multiple specific and long-lasting T cell effects that impose immunity against not only these viruses, but also to SARS-CoV-2.


OK, let me discuss the significance of these findings because they are HUGE. These results show, among other findings, there were memory T cells to SARS-CoV-2 in people who apparently never developed antibodies to this virus and sometimes these people were never even exposed to SARS-CoV-2. These findings with memory T cells along with other studies looking at immune responses to SARS-CoV-2 indicate that somewhere between 40 to 60% of a tested population have at least partial immunity due to prior exposure to common coronaviruses that possess shared antigens with SARS-CoV-2 indicate there is a very strong chance this virus will eventually burn out of its pandemic status on its own through widespread herd immunity, perhaps sooner rather than later. We are seeing evidence of that happening in several countries right now (most notably Italy, Spain, and Sweden) as well as in certain states in the USA, like New York. What these new studies reviewed here provide additional support for is the idea that herd immunity may be much closer than is expected (or reported). Generally, it is believed that 70% of the population must demonstrate immunity to a virus before herd immunity is achieved. But if roughly 40-60% of the population already have some degree of immunity to SARS-CoV-2 as the research currently indicates, that is much closer to that 70% threshold than if the population had started at zero.


Here is something else that is an interesting thought, even though it would never happen. If a coronavirus that causes the common cold produces an immune response that imparts immunity against SARS-CoV-2 because of the presence of several identical antigens could be identified, maybe instead of developing a vaccine with unknown safety and efficacy, we should be instead giving everyone a “cold” by exposing them to this particular common cold coronavirus. Just a crazy thought, right? Maybe not, but it would never happen regardless.

Here is another bit of good news. Another factor coming into play is that SARS-CoV-2 appears to be mutating to a more infectious, but less lethal form. That also bodes well for herd immunity as well as a lower mortality rate. We are still in the first wave in the United States, but perhaps because of more widespread infection here and some countries (e.g., Sweden, Italy, Spain, the UK, etc.) there may not be a second wave that is associated with a high mortality.

I realize that much of what I am sharing here may be controversial because it does not parrot the dominant narrative. So let me balance things out a bit, I do want to address something that should not be a controversy because it too is based upon emerging scientific evidence. I am referring to the importance of everyone wearing a mask in public in areas experiencing high or increasing case numbers. Why wear a mask if you are without symptoms? One of my theories on COVID-19 severity relates to the dosage of viral exposure. Masks may not prevent infection 100%, but it is now undeniable that they do help.  Besides, the real key is to stay away from large doses of the virus, especially if you have one of the risk factors (advanced age, obesity, type 2 diabetes, high blood pressure, chronic respiratory disorder, etc.).

This virus is highly infectious and can be lethal. Do not underestimate this virus or overestimate your ability to defend against it. There is much we do not know about it, particularly long-term effects after the infection is over. So wear a mask when out in public, wash your hands frequently, avoid touching your face, focus on supporting your immune system, and take dietary supplements to boost immune function. Speaking of which, the following nutrients are critical in supporting thymus function and cell mediated immunity:

I also recommend eating at least two serving per day of a carotene-rich food such as green leafy vegetables, carrots, sweet potatoes, spirulina, broccoli, etc. Carotenes are important to protecting the thymus and improving cell mediated immunity. Flavonoid-rich foods are also important, especially berries, citrus, and green tea.

Key References:
  1. Sekine T, Perez-Potti A, Rivera-Ballesteros O, et al. Robust T cell immunity in convalescent individuals with asymptomatic or mild COVID-19. bioRxiv 2020. doi: https://doi.org/10.1101/2020.06.29.174888
  2. Le Bert N, Tan AT, Kunasegaran K, et al. SARS-CoV-2-specific T cell immunity in cases of COVID-19 and SARS, and uninfected controls. Nature. 2020;10.1038/s41586-020-2550-z. doi:10.1038/s41586-020-2550-z

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