The Model is TRUE if you’ve seen it written in Play-Doe 
First of all, I want to say that I am sick of writing and talking about this. It’s been 14 years since I ran across the articles showing the relationship between Lyme and the genetic kind of Autism (the one that co-confers with Neurofibromatosis Type 1).
It’s been 13 years since I scanned in the articles by Paul Duray where he says “these look like Epstein-Barr transformed cells in the spinal fluid of Lyme victims.”
http://www.actionlyme.org/Duray.htm
http://www.actionlyme.org/IDSA_CLINIPATH_DURAY.htm
It’s been 12 years since I first posted an article in the Lyme newsgroup about how bacterial lipoproteins inhibited apoptosis. Edward McSweegan went ballistic on me. March 2004, to be exact. I said, “Hmmm. Sweeg goes ballistic, must be an important thing…”
McSweegan also went crazy and attacked me right after I presented the FDA with the evidence that LYMErix was not a vaccine and that the Dearborn “case definition” for “Lyme disease” was not a consensus among the labs who were “invited” to “participate in the proceedings!”
http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_11.pdf
What else. They attack you when you’re right. It’s a kind of a rule or a Law of Human Physics. When the human will meets the facts, then the slander and mud-slinging begins. If it is a SEVERE, FABULOUS, and ALMIGHTY!! truism or fact, in the USA, they throw you in jail and call you a terrorist.
“How DARE you say Yale distorted the science! You sound like TED KASCYNSKI when you say Yale is abusing technology!! You must be a UNABOMBER CHEMIST to be saying all these true things about Yale!!”
This kind of a mental disorder wherein the truth makes you crazy-furious, is so common now, in America, they say it is not even a mental disorder any more. And that’s thanks to the diabolical delusion called psychology where the frequency (the S in DSM stands for statistics) of debauched and low-life behavior means it’s “common,” and therefore GOOD and “NORMAL!!” “Like the animals!!”
Other “dangerously intelligent” “Unabomber Chemists” you might know of:
“Projects undreamed-of by past generations will absorb our immediate descendants; forces terrific and devastating will be in their hands; comforts, activities, amenities, pleasures will crowd upon them, but their hearts will ache, their lives will be barren, if they have not a vision above material things. And with the hopes and powers will come dangers out of all proportion to the growth of man’s intellect, to the strength of his character or to the efficacy of his institutions. Once more the choice is offered between Blessing and Cursing. Never was the answer that will be given harder to foretell.”
http://teachingamericanhistory.org/library/document/fifty-years-hence/
In a nutshell, the story of “Chronic Lyme” and CFIDS/ME is this: What inhibits apoptosis? BCL2 class genes, be they genetic repeats, promoted by infections like the herpesviruses, or mimicked in their end result / behavior by fungal antigens like those shed by spirochetes or OspA “vaccine” injections…
We, my friends and I, have written easily 30 articles on the very -, explicit -, topic of how OspA causes the same disease we know of as Chronic Lyme. Same headline. How does OspA alone cause the “multi-system disease” known as chronic Lyme? Inhibition of Apoptosis, “arrests the immune process,” causes immunosuppression by BLOCKING what an immune cell would normally do in the presence of a foreign antigen….
We say, “Via immunosuppression, because it is a FUNGAL (TLR2/1) antigen. A lipoprotein. Bacterial lipoproteins of a triacyl type are a bad thing. Bad, bad, bad. Your body can NEVER recover its immune function once whacked with spirochetal antigens like the triacyl lipoproteins.”
And that’s, like, a thing. If a lipoprotein is triacylated, it’s fungal, because it is managed by TLR2 and TLR1. You can’t wish it away or unsay it or hide from it like ILADS and IDSA do, but you can say it backwards. What’s managed by TLR2 and TLR1? Lipoproteins, with 3 acyl groups, which are fungal,… because they have 3 acyl groups and are therefore managed by toll like receptors 2 and 1.
Technically speaking, you’re farked. If you want to find another way to explain to friends and family that you’re farked, permanently, ever since a tick bit your ass, well, be my guest. Maybe we should have a contest.
BUT, I will write about it one more time, because FINALLY it was in the news (but this is old news), that some dudes think they stumbled upon how Epstein-Barr causes cancer – via the immunosuppression mechanism of inhibition the auto-kill genes.
See, the idea isn’t new, 2000:
“This is the first report of the regulation of bfl-1 expression by a viral protein, and this novel finding may thus represent an important link between the EBV oncoprotein LMP1 and its cellular growth-transforming properties.”https://www.ncbi.nlm.nih.gov/pubmed/10864681
It’s old news. You’ve been hearing about it from me for as long as you’ve known me. Okay, exactly 14 years, since 2002. BCL means B Cell Lymphoma.
1) The latest thing on EBV (activated with Malaria, too)?
The way EBV causes disease in its first step, is 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 themselves, or “undergoing apoptosis” when they should kill themselves. Then, EBV can replicate and proliferate within the host cell.
So, the way EBV starts to cause disease (again) is to STOP the immune 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; if you like, search for the term “apoptosis” here: http://www.actionlyme.org/101016.htm
Here is just one report:
1996, Dec; Infection by Candida albicans inhibits apoptosis of human monocytes and monocytic U937 cells.
Infectious microorganisms can differently induce or inhibit apoptosis of immunocompetent effector and host cells. In this study we examined the influence of an infection by Candida albicans (C. albicans) on programmed cell death of monocytic U937 cells and human monocytes. Basal and tumor necrosis factor alpha (TNF-alpha)-induced DNA fragmentation of U937 cells was significantly inhibited by an infection with C. albicans. Enhanced apoptosis of U937 cells, induced by TNF-alpha, caused a diminished candidacidal activity of the effector cells, whereas inhibition of apoptosis by granulocyte-macrophage colony-stimulating factor (GM-CSF) was paralleled by an intensified host defense. Pretreatment of U937 cells or monocytes with the cyclooxygenase blocker indomethacin completely abolished the reduction of DNA fragmentation induced by the yeast. Studying the underlying mechanisms we found that C. albicans induced formation of prostaglandin E2 (PGE2) by U937. Exogenous administration of PGE2 down-regulated apoptosis of U937 or human monocytes to a similar extent as did fungal infection. Activation of protein kinase A by the cAMP analogue 8-bromo-cAMP inhibited U937 apoptosis, as did PGE2. On the other hand, rp-cAMP, a blocker of the cAMP-dependent signal transduction, restored and elevated DNA fragmentation levels down-regulated by C. albicans. U937 cells expressed the bcl-2 protein but the infection with fungi or PGE2 treatment did not increase proto-oncogene expression. Monocytic effector cells may therefore strengthen the defense against C. albicans by an autocrine feedback regulation via a PGE2-dependent, cAMP-transduced inhibition of apoptosis.
http://www.ncbi.nlm.nih.gov/pubmed/8975876
So, imagine, B cells in the Lymph nodes are where 
Borrelia and EBV *BOTH* hang out.
You can verify independently; you really can just “use your Google machine.” Find out if EBV and spirochetes can most reliably be found in B cells and lymph nodes. Do it, since it is a thing you are sure of and can show others.
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.
https://www.ncbi.nlm.nih.gov/pubmed/?term=autism+and+neurofbromatosis
From: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1735052/
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. Epstein-Barr Virus 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 saying this:
“… Whole cell extracts of B. burgdorferi also modulated immune responses but required a much greater quantity of protein than needed for the OspA preparation. The magnitude of modulation was directly dependent on the quantity of OspA. OspA interferes with the response of lymphocytes to proliferative stimuli including a blocking of cell cycle phase progression. Future studies designed to delete the particular region or component of the OspA molecule responsible for this effect may lead to improved vaccine preparations.”
If you want more published data on “Osps or fungal antigens inhibit apoptosis” data it is on an Actionlyme dot org page followed by /101016.htm Search for the term “apoptosis.”
http://www.actionlyme.org/101016.htm
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2) We see the same phenomenon with childhood autism-vaccines: Live attenuated viruses injected together with immune suppressing fungi, *** reactivates the “live, attenuated viruses.”*** [THIS IS IN THE LITERATURE, and old, old news.]
1953 IV. THE RELATIONSHIP OF EPERYTHROZOON COCCOIDES TO THE HEPATITIS VIRUS OF PRINCETON MICE
“In Swiss mice, animals with high natural resistance to hepatitis virus, the pathogenicity of this agent was markedly enhanced by combined infection with eperythrozoa. Eperythrozoa were maintained throughout 18 successive passages in normal Princeton and Swiss weanlings with intact spleens. The combined infection of Princeton mice with eperythrozoa [FUNGAL] and the virus component of Gledhill, Dick, and Andrewes, which is nearly inactive when injected alone, resulted in acute hepatitis with fatal outcome.”
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2136329/?tool=pubmed
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.
2012, Dec, NYTimes; Doctors admit Thimerosal is put in vaccines to prevent fungi:
Vaccine Rule Is Said to Hurt Health Efforts
“But a proposal that the ban include thimerosal, which has been used since the 1930s to prevent bacterial and fungal contamination in multidose vials of vaccines, has drawn strong criticism from pediatricians…. They say that the ethyl-mercury compound is critical for vaccine use in the developing world, where multidose vials are a mainstay…Banning it would require switching to single-dose vials for vaccines, which would cost far more and require new networks of cold storage facilities and additional capacity for waste disposal, the authors of the articles said.'”
http://www.nytimes.com/2012/12/17/health/experts-say-thimerosal-ban-would-imperil-global-health-efforts.html?_r=2&
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.
The Infamous Simon Wessely has had to admit he was WRONG about CFIDS as well as Gulf War Illness, so I am sure we all will feel badly that poor Simon never had an original thought in his life and therefore no PRIDE (“It must be earned!!” says Simon):
“There is now a strong case to be made for a larger trial,” says Simon Wessely of King’s College London, who has treated people using cognitive behavioural therapy. “The belief that [CFS] is all in the mind has been around since the beginning,” he says. “It’s tragic that it might take a study like this to take sufferers seriously.”
https://www.newscientist.com/article/dn27813-antibody-wipeout-found-to-relieve-chronic-fatigue-syndrome/
It’s tragic that Simon never had a brain for thinking, but ran his mouth constantly in hatred of sick people his entire “career” and even had some thrown in jail over fake “threats.” [I personally dont know how anyone can feel threatened when they’re totally wrong about something, must have to do with having an essentially – in its essence – cowardly nature.]
Rituximab 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 whom?
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. …”
You cant make this ^^^ sh*t up.
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.
You already have all this evidence in the criminal charge sheets which we developed 2 years ago.
All the new scientific evidence emerging since 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.
So, in the end, what is the main DiSOrDeR that affects all of America, from the ones with no high school degrees but play “cryme solver” who claim to “put the pieces of the puzzle together” and who run non-profits, to the ones who go around telling the Lyme community they’re “microbiologists with advanced degrees” (but was all along baloney), to regular “MDs” who drink IDSA’s Kool Aid, to the ones who call themselves “LLMDs,” who give you antibiotics to cure a largely chronic EBV/CMV/HHV-6-ish disease, to the “Ivy League,” to NIH and CDC who to this day have never admitted publicly that Pam3Cys never could have been a vaccine and that spirochetes are their own phylum – not to be called “bacteria,” really?
None of them are “Unabomber Chemists?”
A-unabomerosis?
Anti-chemeritis?
“… if they have not a vision above material things. And with the hopes and powers will come dangers out of all proportion to the growth of man’s intellect, to the strength of his character or to the efficacy of his institutions.”
Materialismosis?
VANITY?
You want to know what’s the fekkin DISEASE???
Churchill pegged in in 1932. He said we’d be blinded by what we WANT instead of looking at what is.
He said we may end up offending God, such as with “The Enlightment” where we said Eff You to Creation, like, “Nevermind, we got this,” and ever since, we never did, did we.
Cryme Disease - Unscrambling the CDC's DNA Patent Profiteering Bullshit 