This is the deal. “Lyme disease” means you only have an arthritic knee. “Chronic Lyme disease” is a term that I’m not very fond of, but it’s the term we all use to describe this torture of a wrecked immune system and reactivated viruses.
LYMErix gave people the same disease. This disease is NOT about spirochetes if the LYMErix vaccine gave people the same disease. The vaccine was only an outer surface protein (Osp), the most abundant of them all earning the title of “A”. OspA is a triacylated lipoprotein, Pam3Cys, an endotoxin, a TLR 2/1 agonist- in other words the farthest thing from a vaccine you could possibly get. THAT is how stupid these criminals are.
“Lipoproteins and lipopeptides have repeatedly been shown to act as potent cytokine inducers, interacting with TLR-2, in synergy with TLR-1 or -6. In this study, we show that these compounds also interact with LBP and CD14. We used triacylated lipopeptides, corresponding to lipoproteins of Borrelia burgdorferi, mycobacteria, and Escherichia coli, as well as diacylated lipopeptides, corresponding to, e.g., 2-kDa macrophage activating lipopeptide of Mycoplasma spp.” http://www.jimmunol.org/cgi/content/full/173/4/2683
What is the significance of antigens that are handled by TLR 2/1 (Toll-like Receptors 2 & 1)?
Role of TLR in B cell development: signaling through TLR4 promotes B cell maturation and is inhibited by TLR2.
Hayashi EA1, Akira S, Nobrega A.
“AbstractThe role of TLR4 in mature B cell activation is well characterized. However, little is known about TLR4 role in B cell development. Here, we analyzed the effects of TLR4 and TLR2 agonists on B cell development using an in vitro model of B cell maturation. Highly purified B220(+)IgM(-) B cell precursors from normal C57BL/6 mouse were cultured for 72 h, and B cell maturation in the presence of the TLR agonists was evaluated by expression of IgM, IgD, CD23, and AA4. The addition of LPS or lipid A resulted in a marked increase in the percentage of CD23(+) B cells, while Pam3Cys had no effect alone, but inhibited the increase of CD23(+) B cell population induced by lipid A or LPS. The TLR4-induced expression of CD23 is not accompanied by full activation of the lymphocyte, as suggested by the absence of activation Ag CD69. Experiments with TLR2-knockout mice confirmed that the inhibitory effects of Pam3Cys depend on the expression of TLR2. We studied the effects of TLR-agonists on early steps of B cell differentiation by analyzing IL-7 responsiveness and phenotype of early B cell precursors: we found that both lipid A and Pam3Cys impaired IL-7-dependent proliferation; however, while lipid A up-regulates B220 surface marker, consistent with a more mature phenotype of the IgM(-) precursors, Pam3Cys keeps the precursors on a more immature stage. Taken together, our results suggest that TLR4 signaling favors B lymphocyte maturation, whereas TLR2 arrests/retards that process, ascribing new roles for TLRs in B cell physiology.”
https://www.ncbi.nlm.nih.gov/pubmed/15905502
In short Pam3Cys causes immunosuppression. This kind of damage is not fixed by removing the source of exposure. Killing spirochetes that shed or bleb OspA won’t reverse these kinds of changes to germinal centers (lymph nodes). What “Lyme” patients are left with is a B cell AIDS-like outcome and reactivated viruses and a mixed bag of opportunistic pathogens that cause everything the sun from cancer to dementia to that bone crushing fatigue. “Pam3Cys keeps the precursors on a more immature stage”.
What are B cells and what is their job? From Wikipedia:
“B cells, also known as B lymphocytes, are a type of white blood cell of the lymphocyte subtype.[1] They function in the humoral immunity component of the adaptive immune system by secreting antibodies.[1] Additionally, B cells present antigen(they are also classified as professional antigen-presenting cells (APCs)) and secrete cytokines.[1]
In mammals, B cells mature in the bone marrow, which is at the core of most bones.[2] In birds, B cells mature in the bursa of Fabricius, a lymphoid organ. (The “B” from B cells comes from the name of this organ, where it was first discovered by Chang and Glick,[2] and not from bone marrow as commonly believed).
B cells, unlike the other two classes of lymphocytes, T cells and natural killer cells, express B cell receptors (BCRs) on their cell membrane.[1] BCRs allow the B cell to bind a specific antigen, against which it will initiate an antibody response.[1]“
B cells are what produce antibodies.
Russell Johnson’s patent for the very first Lyme vaccine
US PATENT 4,721,617
“The chronic forms of the disease such as arthritis (joint involvement), acrodermatitis chronica atrophicans (skin involvement), and Bannwart’s syndrome (neurological involvement) may last for months to years and are associated with the persistence of the spirochete. A case of maternal-fetal transmission of B. burgdorferi resulting in neonatal death has been reported. Domestic animals such as the dog also develop arthritis and lameness to this tick-borne infection. For every symptomatic infection, there is at least one asymptomatic infection. Lyme disease is presently the most commonly reported tick-borne disease in the United States.” —
The patent also says:
“The infection may be treated at any time with antibiotics such as penicillin, erythromycin, tetracycline, and ceftriaxone. Once infection has occurred, however, the drugs may not purge the host of the spirochete but may only act to control the chronic forms of the disease.Complications such as arthritis and fatigue may continue for several years after diagnosis and treatment.”
Here is a list of dozens of reports on this being a permanent infection: http://actionlyme.org/BRAIN_PERMANENT.htm
Persistence is old news. We don’t need to talk about it anymore. What we all should be talking about is prosecuting this cryme so that we can move forward and get some treatments for what the true mechanism of this disease is all about. Going around in circles with the same old tired arguments only serves to prolong everyones suffering. We need to save all of these kids and talking about anything other than what the disease really is is hurting everyone. The disease is the cryme. The cryme is the disease. The vaccine caused the same disease without spirochetes. Dig deep and try to answer that question. If the OspA LYMErix vaccine caused the same disease, what does that mean for us who got the disease from a tick bite?
Think about it. Think about the future. Awareness has done nothing. Supporting ILADS has done nothing. So many people can’t afford to pay cash to treat their damaged B cells with antibiotics, so many people can’t even afford Igenex testing in the first place. What about them? What are they supposed to do? “You need to see an LLMD” is not what people who are struggling to keep their electricity on need to hear. Seeing an LLMD is a lost cause for those patients who have spent tens of thousands are still sick. Look at all of the celebrities. All of the money in the world is not helping them. They have done all of the treatments available and are still disabled. Think about it. Why does that happen to them? It’s because of everything that TruthCures talks about. It’s because no one is treating the true mechanism of disease, this post sepsis outcome. Think, think, think and then think some more.
Read the Charge sheets at TruthCures.org and watch the free documentary “Lyme Cryme” on youtube. Sometimes the right direction to go in is the more painful one. We are never going to win this fight without addressing the truth. The truth is not always painless, but that doesn’t make it any less of a truth.
lymecryme.wordpress.com 
This is a fantastic post, thanks!!
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Than you for your encouragement 💐🍀🙏
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