When I first looked at the virus, I saw something horrifying. Deadly, permanent, recurring, and as contagious a disease as the Earth ever had witnessed. From that point forward, I dedicated my time to finding, and sharing, treatments and cures, for the preservation and life of all humanity. Little did I know then of the enormous powers lined up against us.
Fortunately, as the work of some great leaders in medicine eventually discovered and told the world, the infection was not to be permanent, Herpes-like, after all. An overlooked aspect of our immune system, namely CD8+ T-cells, provided an immunity of last resort, against a virus that was otherwise comprehensively cloaked against immune detection.
We have now lost that luxury.
To begin this article, I should first explain to you, briefly, some various types of immunity that we are possessed of. Each of them plays an important role, and each of us have slight differences that affect our susceptibility to infection, morbidity and death.
Broadly, I will describe the first category of immunity, innate immunity. This covers such immune cells as macrophages, neutrophils and others. These are blunt force instruments, responding to cytokine and complement signals of infection early in the process to phagocytose foreign pathogens, signal infected cells to destroy themselves, activate stronger immune responses, and release cytotoxic chemical soup to mechanically destroy infected cells, also catching uninfected cells in the crossfire.
The second category, as you probably know, is adaptive immunity. This is, broadly, the antibody response. It is mediated by dendritic cells, CD4+ T-cells and B cells among others, which capture proteins from phagocytosed virions, study them, and by a process of trial and error, produce antibodies which bind to the recognized protein fragments. When a live pathogen that matches a previously processed protein is detected, the body releases a flood of antibodies. Those antibodies bind to the pathogen and act as hooks to enable macrophages to more easily destroy the pathogen. This form of immunity is largely irrelevant to this discussion.
The third category, very minimally described in the literature as a cohesive field, is cytosolic immunity. This covers such intracellular detection and defense mechanisms as toll-like receptors, interferon-stimulated genes, endolysosomes and protein kinases. These form an integral link in the various mechanisms which activate the broader immune system, and it is here that our problem begins.
MHC stands for major histocompatibility complex, of which there are two kinds, MHC-I and MHC-II. When a cell is infected, and cytosolic sensors detect it in the endosome upon infection, the endosome fuses with a lysosome to become an endolysosome, MHC proteins being produced in the endoplasmic reticulum, and the nucleus begins producing interferon to warn neighboring cells to be on guard for infection. The viral protein is dissolved into chunks, and MHC-I is transported into the endolysosome. This protein attaches to those chunks of viral protein, and carries them to the surface, where T-cells can bind to it and obtain a sample of the viral protein to begin building immunity (when this fails, it’s a problem.) MHC-I also acts as a binding site for effector CD8+ T-lymphocytes. Upon binding to an MHC-I protein on the surface of an infected cell, the effector CD8+ cell will then destroy the cell. This action is of vital importance to the clearing of COVID-19 infection, as via the ACE2 receptor, the virus infects immunoprivileged cells that no other component of the immune system is permitted to attack. This mechanism evolved in order to protect us from our immune system damaging critically important and irreplaceable parts, such as nerves and gonads.
Stepping back: The SARS-CoV-2 virus uses the importin alpha-beta complex to import the ORF6 protein into the cell nucleus, which interferes with the action of MHC-II, among others. This is one aspect of its cloaking function – the other being glycosylation of antigens – which interfere with antibody recognition and binding, and prevents a cell from releasing interferon particles to warn its neighbors to defend against imminent infection. This delays, but does not prevent, the formation of adaptive immunity.
MHC-I has, until this time, been only mildly downregulated in this process, which has enabled clearance of infected, immunoprivileged cells via cytotoxic CD8+ T-lymphocyte interaction, and made vitamin D3 a very useful adjunct in the treatment of COVID-19, due to its effect increasing the number of effector CD8+ cells, enabling more rapid and thorough clearance of infected cells.
New research, however, has identified a mutation of SARS-CoV-2 which is now able to escape the grasp of MHC-I in the endolysosome, and thus impair the cell surface presentation of MHC-I protein. The viral protein has simply mutated, by random evolutionary chance, very likely under hyper-evolutionary pressure from vaccine-induced IgG and IgM antibodies, such that it is possessed of a shape that the protein complex is unable to grasp and hold. The presence of such antibodies in the blood impairs the ability of the virus to spread from an infected cell, but they do not target the infected cells themselves; only the cell’s presentation of MHC-I is able to identify it as infected and cause it to be targeted for destruction. Without being able to present MHC-I, immunoprivileged cells may remain permanently infected, budding out endless virions (rather than bursting their host cell – an important distinction), keeping the body in a hyper-immune state and causing as yet unknown pathologies.
The implications of this are potentially far reaching. ACE2-mediated infection of immunoprivileged cells, very uncommon for viruses, means that cytotoxic CD8+ T-lymphocytes are the only means, aside from incredibly damaging and indiscriminate cytokine storms, by which infected immunoprivileged cells can be either instructed to self-destruct or be mechanically destroyed. Without this mechanism, and considering that the viral proteins ORF8, ORF6 and ORF3b already inhibit interferon and MHC-II production inside the cell, and that there are multiple N-linked glycosylation sites on the spike protein, which cloak the virion in sugar to protect it from antibody recognition and binding – we may no longer have any available means to naturally clear an infection without therapeutic intervention.
This would be bad news, but not the worst news, if our medical system wasn’t so hopelessly incompetent and corrupt that extraordinarily useful therapeutics such as ivermectin are pushed by the wayside, lied about in media[34-37], and suffer in reputation from the concoction of fake science and rigged trials by the pharmaceutical interests that apparently wish to prolong the pandemic as long as possible. Unfortunately, our medical system is hopelessly incompetent and corrupt. The consequences of this mutation will be dramatically amplified by our utterly insane “wait and see” policies against early treatment, which will likely manifest in a dramatic acceleration of COVID-related hospitalizations, closures, lockdowns, and of course a renewed emphasis on mass vaccination.
From the point of view of the COVID-19 disease itself, what we may begin seeing in patients will be much more in line with what we saw very early on in the pandemic. With the virus perpetually present inside immunoprivileged cells, and still in possession of the gp120 HIV spike protein, it is highly likely that CD4+ depletion, cytokine storms and pneumonia will occur in a much higher proportion of patients. There are also likely to be more deleterious effects in the brain as CD4+ cells pyropoptose in response to CD4 receptor binding, which is a classic symptom of late-stage AIDS. Recoveries will take longer, and while steroids, blood thinners and targeted immunotherapies such as tocilizumab may be able to temporarily ameliorate symptoms, the use of effective antivirals will become absolutely mandatory.
It is ironic that this mutation is highly likely, although by no means proven, to have resulted from hyper-evolutionary pressures applied by vaccines. The presently available vaccines, to their credit, appear to be mostly effective in the prevention of severe disease and mortality – for now. These vaccines work by providing IgG and IgM, but not IgA antibodies. This is a crucial shortcoming; IgA antibodies reside in epithelial tissues and prevent initial infection, whereas IgG and IgM antibodies patrol the blood and attack free virions, reducing the innate inflammatory immune response and inhibiting further spread of the virus throughout nearby tissues. However, without destroying infected cells, this simply means that the virus is remaining in place, replicating and mutating. Eventually, a random mutation occurs which allows the virus to evade those IgG and IgM antibodies, and by virtue of then becoming able to spread, that virus is quickly selected by evolution and becomes the dominant strain. As CD8 has been the primary mechanism by which infected cells are destroyed, the virus’ evasion of MHC-I and CD8 immunity is likely an evolutionary response to being trapped in a cell and eventually destroyed; now, the host cells will no longer be destroyed.
This is not a unique scenario. Marek’s disease, a lymphoma virus disease in chickens, is the best known example of leaky vaccines causing evolutionary escape. Long story short, the original virus was relatively mild, until flocks of chickens were vaccinated with leaky vaccines that, while preventing the chickens from dying, did not prevent infection. The virus engaged in an evolutionary arms race against the vaccines, which required frequent updates, and became more infectious and lethal over time. Eventually, the virus became so lethal that any unvaccinated chicken was certain to die if infected; the vaccine became the only means by which a flock of chickens could expect to survive an outbreak.
Humanity is at a crossroads. If we continue mass vaccination with these half-measure vaccines, we will see more, more infectious and deadlier strains of SARS-CoV-2 evolve. It is not a question of if; it is a question of when. Unlike other times in history, we are fortunate enough to have discovered a plentiful, extraordinarily safe and effective therapeutic[55-68], in ivermectin (among a number of other very promising therapeutics.) Ivermectin is, for a variety of reasons,[21,69-72] highly unlikely to cease being curative, without concerted and deliberate effort to engineer gain of function into a new virus. The people that think they’re being responsible and contributing to “herd immunity” – they are not. The only benefit of the vaccines is that they will likely, temporarily, protect from severe disease and mortality, until the next strain emerges. Ivermectin can also accomplish this, with a far lower risk profile, and without inducing an evolutionary arms race against the virus. It has been endorsed and put into practice by many governments, to great results; others, including our own, are actively sabotaging it, publishing fake trials, fake news, and fear, just as was done to HCQ.
The people that have been buying the official story all along – the mask Karens, the Fauci fans, the hopelessly suckered TV watchers – they, generally, are the ones most eager and likely to be vaccinated. While their sanctimonious disrespect for the work of many of the most skilled scientists and doctors in the world has cost many lives, mostly it has just been their own, having failed to study what works, and finding themselves at the mercy of our corrupt medical system. By adhering to religious scientism, failing to even acknowledge what the authorities have fully admitted about the potential for harm, and by taking the vaccines, they are now becoming an active danger to our collective health and well being. The vaccinated people, slowly gaining their own special status with vaccine passports, reserved beach seats and God knows what else is coming – they are Typhoid Maries, creating and cementing the existence of an ever-increasingly deadly disease in our midst, and dooming everybody to death, vaccinated or not, when eventually the latest shot can no longer prevent the horrifying disease of this hyper-evolved bioweapon. We must educate those people, and we must do it soon, because our health authorities are not about to abort the multi-billion dollar push for widespread vaccination. Effectively, the people who have been vaccinated are those who society most needs to now adopt pre-exposure prophylactic protocols with the antiviral drug of their choice; they are the ones incubating and spreading deadly disease, not the unvaccinated.
This is still in the early stages. We are now starting to see mutations such as this emerge. More vaccines to counter them will follow, and deadlier, harder to treat strains will follow those. We must break this cycle now. Support the use of ivermectin. Tell your friends, family, colleagues, communities, doctors, local governments, and anybody else that will listen, that we have an alternative to this incipient hellscape. Buy an ivermectin shirt, hat or mask – it won’t be quickly forgotten! Take your local health authority to court and obtain a declaration that ivermectin is an effective treatment under Section 564 of the FDA Act. Whatever you can do, now is the time to start doing it.
Time is rapidly running out.
A note of optimism: in the beginning of the pandemic, the scenario described above was precisely what was feared. The crucial impact of effector CD8+ T-cells was completely overlooked, which brought mortality and morbidity significantly down, and allayed fears of permanent, recurring infection. With the loss of CD8 function, the situation does look grim; however, as with any mutation, we do not yet fully understand it, and the evolutionary tradeoff necessary for this new cloaking function may have resulted in the loss of another function, enabling an as-yet unknown mechanism to still effect clearance. Millions of years of evolution have made us pretty resilient. Let’s hope this just turns out to be another blip on the radar.
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