Saturday, November 19, 2016

LYME IS


The Model is TRUE if you've seen it written in Play-Doe :)
http://www.actionlyme.org/EAT_OSPA_GO_LIMP.jpg
1) You saw the latest thing on EBV (activated with Malaria, too)? (See ActionLyme.org near the top if you missed it).
The way EBV causes disease is in the first step, INHIBITION of the "auto-kill" kinases (apoptosis means, "I will kill myself," says the cell, "if I am infected with something I cant control"), or BCL2 (stands for "B Cell Lymphoma"- clue) genes.
I will say that again: The way EBV causes disease, in the first step, is that it *stops* the cells infected by it, from killing itself, or "undergoing apoptosis."
So, in a way, the way EBV starts to cause disease (again) is to STOP the cell from killing itself, which is what the BCL2 class genes do - the BCL2 class genes say "DO NOT COMMIT SUICIDE"; it's like having TOO MUCH BCL2 gene expression. Then it starts replicating and pouring out little EBV-babies.
OspA or other fungal antigens do the same thing. They *act* like too much BCL2, or cause the cell to not kill itself. Fungal antigens INHIBIT APOPTOSIS. [You can verify that independently, it's also well-reported in the scientific literature.]
So, imagine, B cells in the Lymph nodes are where both Borrelia and EBV *BOTH* hang out. [You can verify independently.]
You can also have a genetic abnormality where you have a duplication (imagine a rope lying on the ground with a loop in it, and that loop recombines with a straight strand of DNA). This is called a reversed-duplication, and happens in "nerve overgrowth syndromes" (that's a thing) such as the kind of Autism Einstein had, and where Neurofibromatosis co-occurs with "the Autism Spectrum," - also now a well known thing.
Why. Too much BCL2, or not enough "natural neurodevelopmental synaptic pruning." These kinds of Autism kids have too many nerves, or tumorish nerve endings (Neurofibroma), and large brains.
Why. They have a reversed duplication of a BCL2 class gene, which STOPS the nerve cells from dying on schedule.

So, too much BCL2 *STOPS* the normal process of a cell killing itself when it should. EBV also PROMOTES the expression of BCL2 class genes (assuring that it can continue to replicate, which is BAD), which is bad. And the Osps, like OspA *ALSO* tell the cell not to kill itself. You saw even Gary Wormser say this.
If you want that "Osps or fungal antigens inhibit apoptosis" data it is on an Actionlyme dot org page followed by /101016.htm Search for the term "apoptosis."
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2) Same thing with childhood vaccines: Live attenuated viruses injected together with immune suppressing fungi, *** reactivates the "live, attenuated viruses."*** [THIS IS IN THE LITERATURE.]
3) This is a real thing. We see it everywhere. We hear about it in the Humira and Stelara commercials (immune-suppressing) - they talk about the "risk of LYMPHOMA" which comes from reactivated EBV - which is nearly the first thing if not 100% the first thing that happens in all kinds of immunosuppression cases.
Because there are so many parallel models, we call that an "Occam's Razor" ("it *MUST* be *THIS*").
4) In AIDS, people die of the opportunistic infections, like Karposi's scarcoma, which is caused by what? A HERPES VIRUS!!
Immunosuppression ALWAYS results in the reactivation of latent viruses.
5) How about organ transplant victims? Yes, "risk of lymphoma (EBV)" because they have to take immune suppressing drugs. Happens all the time. A lot of transplant patients end up with cancer, this is a well-known thing...
6) Hospital Sepsis? YES, well known now: reactivated latent herpes viruses. (Dual or multiple infections, cytokine storm, boom, the immune response STOPS to keep the human alive.)
Fungi cause immunosuppression. Cant have that with live viruses in the vaccine vial.
LYMErix was fungal. The diseases - Lyme and LYMErix - are mainly caused by the reactivated herpesviruses (Great Imitator was really the Great Detonator of EBV, et al.)
7) Thimerosal was *EXACTLY* invented to prevent LYMErix.
They call mercury (Thimerosal) a "preservative." Why. Because it prevents FUNGAL growth, which is the worse immune suppressor.
True Story.
8) Rituximab is a mab (monoclonal antibody) that targets CD20 on B cells. It is a "B-cell depleter." Where does EBV hang out? Right. B cells.
It seems to help the CFIDS/ME people. Why. Because THAT disease is also an immune suppression disease, spoken of as Post-Sepsis Syndrome, and spoken of by who?
WHO?
9) ANTHONY FAUCI in a 1995 patent (5,696,079).
"....Illustrative of specific disease states in treatment of which the present invention can be applied are HIV infection and other diseases ***characterized by a decrease of T-cell immunity, for example, mycobacterial infections like tuberculosis and fungal infections such as cryptococcal disease.*** This method also can be used in the treatment of secondary infections that occur in patients with suppressed immune systems, such as the opportunistic infections that occur in AIDS patients. ..."
MYCO or fungal diseases, well known to cause immune suppression. They put Thimerosal in vaccines to prevent fungal antigens like LYMErix or the Osps on the shed blebs of spirochetes, all spirochetes, Syphilis too.
Stop making me say the same gallblammed thing every day. You already have all this evidence in the criminal charge sheets which we developed 2 years ago. The new evidence only supports this model, and NOTHING has detracted from this model.
Something is considered TRUE if it passes the requirements of the Scientific Method, which states that the model must repeat, or is VALID. Not only does the model of Pam3Cys as a fungal antigen causing immunosuppression repeat, we show the science proves this phenomenon occurs in other disease conditions, and with other drugs and vaccines.
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