Plague by design - Paradoxical Acquired Immune Dysfunction hypothesis
A introduction to the complexity of a jab
For a few weeks I have been trying to simplify this subject, but it's too complex, took me months of 16 hours a day, interdisciplinary research, and the help of someone 3x more intelligent than me to reach this point, so I will just go dividing into multiple parts.
And for the record, the other person who wishes to remain anonymous deserves more of the credit than I.
For half of 2021, I kept looking at SARS-CoV-2 as not merely as a viral disease, but a metabolic one, so my focus was on finding the causes of systemic Ferroptosis and it's propensity for being sugar hungry, the so-called Warburg Effect.
Feeling like we did the research years ago now… at a point, by sheer accident while looking into the possible pathways we stumble into specific cell responses to the virus, and at the same time an interview with Dr. Ryan Cole went viral, his findings, via different methods, the same.
In lots of patients, he was seeing a huge increase in cancer and their CD8 levels dropping vertiginously. He said, “It looks like reverse AIDS”. Mere days after, a paper went viral, showing how strong, good, broad, and lasting the immune response to the mRNA vaccine was. 1
Pay close attention to this graphic, because it says it all. From little CD8 response to negative after 6 months. The signal on social media is easy to track, with thousands saying their CD8 levels tanked after the jab. Here is a simple and good explanation of what exactly are CD8 cells 2 . It's how your body fights foreign entities. It's also how your body suppresses chronic infections (important later on).
Reduction of CD8+ T cells and increase in classic monocyte contents were exemplary. Moreover, scRNA-seq revealed increased NF-B signaling and reduced type I interferon responses, which were confirmed by biological assays and also had been reported to occur after SARS-CoV-2 infection with aggravating symptoms. Altogether, our study recommends additional caution when vaccinating people with pre-existing clinical conditions, including diabetes, electrolyte imbalances, renal dysfunction, and coagulation disorders.
Surprisingly, type I interferon responses, which had been linked to reduced damages after SARS-CoV-2 infection and milder symptoms, appeared to be reduced after vaccination, at least by 28 days post the 1st inoculation. This might suggest that in the short-term (1 month) after vaccination, a persons immune system is in a non-privileged state, and may require more protection. 3
From another paper 4 .
There was a firm correlation between the highest values of inflammation indicators with the decrease in percentage of CD8 T-lymphocytes. This effect was not seen with CD4 cells.
Suboptimal SARS-CoV-2−specific CD8+ T cell response associated with the prominent HLA-A*02:01 phenotype 5(ignore the authors opinion on vaccination and CD8).
Old people won't get much immunity from either infection, but especially vaccination. 6
IMPORTANCE Cytotoxic T cells are responsible for the elimination of infected cells and are key players in the control of viruses. CD8+ T cells with an effector phenotype express cytotoxic molecules and are able to perform target cell killing. COVID-19 patients with a mild disease course were analyzed for the differentiation status and cytotoxic profile of CD8+ T cells. SARS-CoV-2 infection induced a vigorous cytotoxic CD8+ T cell response. However, this cytotoxic profile of T cells was not detected in COVID-19 patients over the age of 80 years. Thus, the absence of a cytotoxic response in elderly patients might be a possible reason for the more frequent severity of COVID-19 in this age group than in younger patients.
This paper will be timeless in a few years. 7
Common Variable Immunodeficiency Disorders, T-Cell Responses to SARS-CoV-2 Vaccines, and the Risk of Chronic COVID-19
Write that disorder's name on paper. Keep that in mind. The one below, the bold part is the main one.
During hospitalization, circulating counts of T lymphocytes, CD4+ T cells, and CD8+ T cells were lower, whereas neutrophil proportion, neutrophil/lymphocyte ratio, and the circulating levels of interleukin-6, C-reactive protein, and procalcitonin were higher, in pneumonia patients than in pneumonia-free patients. CD8+ lymphocyte count in pneumonia patients did not recover when discharged 8
There was a firm correlation between the highest values of inflammation indicators with the decrease in percentage of CD8 T-lymphocytes. 9
This entire paper mentions the low CD8 response of vaccinated individuals when presented with the spike protein, and no against the N (to be expected). 10
The response of vaccine-elicited CD8+ T cells to spike peptides was weaker, and mostly apparent only after the second dose (Figure 1B, top right). As expected, vaccination did not elicit T cells able to respond to nucleocapsid peptides
Widespread SARS-CoV-2 mutation escapes vaccine- and infection-induced CD8 T-cell responses
Sustained cellular immune dysregulation in individuals recovering from SARS-CoV-2 infection
Changes in T cell activation/exhaustion in nonhospitalized patients were found to positively correlate with age. Severely infected individuals had increased expression of activation and exhaustion markers. These data suggest a prolonged period of immune dysregulation after SARS-CoV-2 infection, highlighting the need for additional studies investigating immune dysregulation in convalescent individuals. 12
T-cell exhaustion may limit long-term immunity in COVID-19 patients
New data suggests people who develop severe COVID-19 symptoms may be better protected from reinfection. According to the investigators, the memory T cells of people who experience mild COVID-19 symptoms show the molecular signs of exhaustion and therefore could have a reduced ability to fight reinfection. 13
The paper below is not related to the pandemic, but it's fairly important on its own, and unbelievably important later on, when we discuss Toll-Like Receptors a little.
B cell depletion impairs vaccination-induced CD8+ T cell responses in a type I interferon-dependent manner
Conclusions Depending on the stimulus, B cells can modulate CD8+ T cell responses. Thus, B cell depletion causes a deficiency of de novo antibody responses and affects the efficacy of cellular response including cytotoxic T cells. The choice of the appropriate vaccine to vaccinate B cell-depleted patients has to be re-evaluated in order to efficiently induce protective CD8+ T cell responses. 14
Anyone with any interest in this hypothesis and the systemic adverse effects of the current immunization efforts should read this paper. Among all the papers, this one is one of the most important ones, with the most ramifications, a fairly complex analysis of a variable most is ignoring. Co and chronic infections.
Because in the end, this is what Corona truly is. The Everything disease and pathology acceleration.
CD8+ T-Cell Deficiency, Epstein-Barr Virus Infection, Vitamin D Deficiency, and Steps to Autoimmunity: A Unifying Hypothesis
CD8+ T-cell deficiency is a feature of many chronic autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus, Sjögren's syndrome, systemic sclerosis, dermatomyositis, primary biliary cirrhosis, primary sclerosing cholangitis, ulcerative colitis, Crohn's disease, psoriasis, vitiligo, bullous pemphigoid, alopecia areata, idiopathic dilated cardiomyopathy, type 1 diabetes mellitus, Graves' disease, Hashimoto's thyroiditis, myasthenia gravis, IgA nephropathy, membranous nephropathy, and pernicious anaemia. It also occurs in healthy blood relatives of patients with autoimmune diseases, suggesting it is genetically determined. Here it is proposed that this CD8+ T-cell deficiency underlies the development of chronic autoimmune diseases by impairing CD8+ T-cell control of Epstein-Barr virus (EBV) infection, with the result that EBV-infected autoreactive B cells accumulate in the target organ where they produce pathogenic autoantibodies and provide costimulatory survival signals to autoreactive T cells which would otherwise die in the target organ by activation-induced apoptosis. Autoimmunity is postulated to evolve in the following steps: (1) CD8+ T-cell deficiency, (2) primary EBV infection, (3) decreased CD8+ T-cell control of EBV, (4) increased EBV load and increased anti-EBV antibodies, (5) EBV infection in the target organ, (6) clonal expansion of EBV-infected autoreactive B cells in the target organ, (7) infiltration of autoreactive T cells into the target organ, and (8) development of ectopic lymphoid follicles in the target organ. It is also proposed that deprivation of sunlight and vitamin D at higher latitudes facilitates the development of autoimmune diseases by aggravating the CD8+ T-cell deficiency and thereby further impairing control of EBV. The hypothesis makes predictions which can be tested, including the prevention and successful treatment of chronic autoimmune diseases by controlling EBV infection. 15
I could keep citing papers, and studies and using cool images, but I suspect my first point is made. A part of this virus is the immune response it elicited even when inactivativated and the novel vaccines all cause a substantial drop in one of the most important aspects of your immune system. This is also called immune skew, when one side suddenly drops, the other dominates, and the ratio between your immune cells is skewed.
Ad this is where all problems really start. Because yes, the transient death of your natural killer cells is not your biggest worry yet.
I will be making these short to make them easier to understand so this one ends here.
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