Killer virus or killer vaccine?
by
Fred Teunissen, PhD. and *Robert Gorter, MD, PhD. ·
April 22nd, 2021
Is the killer virus going to make large-scale victims by developing nasty variants? Or is it precisely the vaccinations that will lead to a wave of deaths and will then be falsely attributed to a mutated killer virus?
This is the question that the corona debate is currently focusing on
The so-called mean variants are not only warned for by the WHO and national health authorities but now also by the rising number of doctors, who until now have been very critical of the entire corona approach.
These critical doctors believe that the vaccinations will corner the virus and that it will then develop dangerous variants that will hit the unvaccinated especially hard.
It is therefore logical that they strongly urge to stop vaccinating immediately. Among them the renowned British physician and author Vernon Coleman.
Shaky virus belief
The well-established mainstream group does not see the vaccinated as the source of the variants, but rather the unvaccinated and potentially also animals, because they claim that viruses can pass from animals to humans (and vice versa) and then can become a kind of turbo hazard / catalytic converter.
Both directions are firmly rooted in the belief in the contagiousness and pathogenicity of some viruses.
That this basis is particularly shaky may be clear, after a year of corona discussion.
The existence of a SARS-COV-2 virus has still not been proven. Till today, the CDC in the USA was still not able to deliver a complete and viable SARS-CoV-2 virus for sequencing. See what Jon Rappoport wrote about this in his blog in April 2021:
“These researchers create a soup in a dish in a lab. They put toxic chemicals and drugs in the soup. They put monkey and/or human cells in the soup. There is much other genetic material in the brew—including, supposedly, the virus. The cells, starved of nutrients, and poisoned, begin to die. The researchers then assert THE VIRUS must be doing the killing. Therefore, the virus IS in the soup and it is deadly.”
But there is no evidence that the un-isolated virus is in the soup, and there is no evidence it is doing the killing.
On the back of these absurdities, a declaration is made: there is a pandemic, and the cause is a virus, named SARS- CoV-2.
Going even further, the researchers claim they’ve mapped the genetic sequence of the virus. Based on what? Compared to what? They don’t have an isolated specimen of the virus. How do you sequence something you don’t have? You don’t.”
This puts all assumptions about killer variants on quicksand. After all, if that of which something is a variant has not been demonstrated, how can there be such a thing as a dangerous variant?
The perfect killing machine
Other experts make an even more ominous sound. They foresee that it is precisely the vaccinations that will lead to a major disaster. And not because of “variants”, but because of the biotechnical design of the mRNA vaccines themselves. These produce autoimmune reactions, without a stop button built-in, they say.
This means that the body is going to break down itself and that the vaccinated person has to fight an unequal battle. After all: the brake is missing.
Dr.Gorter: another, publically never-discussed but worrisome issue is the fact that mRNA vaccinations are never 100% pure: a certain percentage is divergant. Nobody knows exactly which proteins will be manufactured by ribosomes initiated by these divergant RNA molecules.
Dr. Sherri Tenpenny is a physician, osteopath, and director of a holistic medical center in Cleveland, Ohio (USA). She calls the Covid vaccines a perfect killing machine. Not only because there are not many (or perhaps none) remedies for it in a traditional medical sense, but also because it kills very slowly. She mentions a period ranging from seven months to a few years. Making the link to the covid injections afterward will then be difficult.
Dr. Robert Gorter:
The adaptive immune system in mammals and humans has two independent but tightly collaborating systems:
- The Humoral System
- The Cellular System
Adaptive Immunity – Humoral and Cellular Immunity
Humoral immunity is also called antibody-mediated immunity. With assistance from helper T cells, B cells will differentiate into plasma B cells that can produce antibodies against a specific antigen. The humoral immune system deals with antigens from pathogens that are freely circulating, or outside the infected cells. Antibodies produced by the B cells will bind to antigens, neutralizing them, or causing lysis (dissolution or destruction of cells by a lysin) or phagocytosis.
Cellular immunity occurs inside infected cells and is mediated by T lymphocytes. The pathogen’s antigens are expressed on the cell surface or on an antigen-presenting cell (also dendritic cells are a very good example of antigen-presenting lymphocytes). Helper T cells release cytokines that help activated T cells bind to the infected cells’ MHC-antigen complex and differentiate the T cell into a cytotoxic T cell. The infected cell then undergoes lysis.
Innate (non-specific) vs. Adaptive (specific) Immune Response
The first line of defense against non-self pathogens is the innate, or non-specific, immune response. The innate immune response consists of physical, chemical, and cellular defenses against pathogens. Cytokine releases are just one example of this mechanism. The main purpose of the innate immune response is to immediately prevent the spread and movement of foreign pathogens throughout the body.
The second line of defense against non-self pathogens is called the adaptive immune response. Adaptive immunity is also referred to as acquired immunity or specific immunity and is only found in vertebrates. Lower animals (non-vertebrates) must rely on eosinophils for their defense system against pathogens. Eosinophils invertebrates play a role in allergic reactions and in parasitic infections. The adaptive immune response is specific to the pathogen presented. For each pathogen, a new adaptive immune response is augmented. The adaptive immune response is meant to attack non-self pathogens but can sometimes make errors and attack itself. When this happens, autoimmune diseases can develop (e.g., lupus, rheumatoid arthritis, thrombosis).
The hallmark of the adaptive immune system is the clonal expansion of lymphocytes. Clonal expansion is the rapid increase of T and B lymphocytes from one or a few cells to many millions. Each clone that originates from the original T or B lymphocyte has the same antigen receptor as the original and fights the same pathogen.
While the innate immune response is immediate, the adaptive immune response is not. However, the effect of the adaptive immune response is long-lasting to usually life-long lasting, highly specific and is sustained long-term/life-long by memory T cells.
What are ribosomes?
Ribosomes are macromolecular “factories”, found within all living cells that perform biological protein synthesis (mRNA translation). Ribosomes link amino acids together in the order specified by the codons of messenger RNA (mRNA) molecules to form polypeptide chains. Ribosomes consist of two major components: the small and large ribosomal subunits. Each subunit consists of one or more ribosomal RNA molecules and many ribosomal proteins. The ribosomes and associated molecules are also known as the translational apparatus.
While examining the animal and plant cell through a light microscope, one might have seen numerous organelles that work together to complete the cell activities. One of the essential cell organelles are ribosomes, which are in charge of protein synthesis; also the production of antibodies.
The ribosome is a complex made of protein and RNA and which adds up to numerous million Daltons in size and assumes an important part in the course of decoding the genetic message reserved in the genome into protein. Ribosomes can “float” in the cytoplasm or be fixed to membranes.
How does normally build the immune system immunity?
When a pathogen (virus) enters the body, there is an immediate and local immune response by the innate immune system. The first line response is activated immediately.
Antigen-presenting cells are vital for effective adaptive immune response, as the functioning of both cytotoxic and helper T cells is dependent on APCs. Antigen presentation allows for the specificity of adaptive immunity and can contribute to immune responses against both intracellular and extracellular pathogens. It is also involved in the defense against tumors. Some cancer therapies involve the creation of artificial APCs to prime the adaptive immune system to target malignant cells.
Dendritic cells (DCs)
Dendritic cells have the broadest range of antigen presentation and are necessary for the activation of naive T cells. DCs present antigen to both helper and cytotoxic T cells. They can also perform cross-presentation, a process by which they present exogenous antigen on MHC class I molecules to cytotoxic T cells. Cross-presentation allows for the activation of these T cells. Dendritic cells also play a role in peripheral tolerance, which contributes to the prevention of auto-immune disease.
Prior to encountering foreign antigens, dendritic cells express very low levels of MHC class II and co-stimulatory molecules on their cell surface. These immature dendritic cells are ineffective at presenting antigen to T helper cells. Once a dendritic cell’s pattern-recognition receptors recognize a pathogen-associated molecular pattern, the antigen is sampled and phagocytosed and the dendritic cell becomes activated, upregulating the expression of MHC class II molecules. It also upregulates several co-stimulatory molecules required for T cell activation, including CD40 and B7. The latter can interact with CD28 on the surface of a CD4+ T cell. The dendritic cell is then a fully mature professional APC. It moves from the tissue to lymph nodes, where it encounters and activates T cells.
Then, antigen-presenting cells (like dendritic cells) arrive and take antigen samples (in principle that of a biopsy) of the intruding pathogen and transport the antigen sample to the lymph node where the antigens samples are presented to Natural Killer (NK) cells, T Memory cells, and B cells.
B cells create mRNA to be sent to the ribosomes to initiate specific antibody production against the pathogen(s). Then, through the cellular immune system with its memory, life-long immunity is being guaranteed.
Through the years, antibody production of a specific pathogen might slow down (like in the case of measles) but after exposure to the pathogen, within a matter of hours, full production of antibodies is being jumpstarted again and neutralize the pathogen.
What could possibly go wrong with synthesized mRNA vaccinations?
As natural mRNA is composed by and under the direction of the adaptive (cellular) immune system where memory cells play such an important role in guaranteeing life-long immunity, the synthesized mRNA in the current anti-SARS-CoV-2 vaccines circumvent the adaptive immune system completely, as here explained. The synthesized mRNA targets the ribosomes directly and initiates antibody production. But this injected synthesized mRNA is being consumed as the adaptive immune system “does not even know” (so to speak) that synthesized mRNA entered the ribosomes. Therefore, the antibody production ends after six to eight months and a new vaccination with synthesized mRNA must take place; and so on; and so on.
That explains why natural immunity with its memory cells is life-long and injections with synthesized mRNA need to be repeated life-long.
Injections with synthesized mRNA will turn out to be a Box of Pandora
*Robert Gorter, MD, PhD, served as a faculty member more or less simultaneously six major universities in three continents between 1975 and 2020. Robert Gorter graduated from the University of Amsterdam, The Netherlands, and is a licensed and practicing physician since 1971 till today. Gorter has specialties in Medicine, Oncology, Immunology, Virology, Biostatistics, Public Health, Tropical Medicine, and Translational Medicine.