170622 email – Some NIH Employees to Subpoena for the Prosecution.

To: Judiciary Committee Reps and others.
Cc: The Crew

Subject: NIH themselves said OspA alone, as a fungal toxin, is responsible for the immunosuppression outcome of Lyme (Marques, Martin, Dorward)

Date: Jun 22, 2017 4:54 AM
Greetings,
I thought it would be worthwhile to point out that the NIH used to have a “MS and Lyme” division of the National Institute of Neurological Disorders and Stroke (NINDS), where a man named Roland Martin and a lady named Adrianna Marques were tasked to discover how Lyme caused MS. Note that Lyme arthritis or the genetically linked tendency to have arthritis alone, is very different from Multiple Sclerosis. In fact, they never occur together as a general rule in Medicine.
As we showed you with the handout we (truthcures.org) gave you, ONLY the HLA-linked or genetically linked tendency to have an arthritis response to Lyme or the LYMErix vaccine (per Allen Steere, and hence the class action lawsuits against SmithKline (see Sheller.com), is allowed to be a “case” of “Lyme disease,” per the Dearborn scam put on by the very people who own the patents – CDC staff, mainly.
Barbara Johnson, Alan Barbour. Johnson ran the Dearborn scam. Please download a copy of the Dearborn booklet so you can see that none of the labs invited to participate in the Dearborn stunt were listened to, they were all blown off when they said this proposal, wherein the case definition was falsified such as to only detect high concentrations of antibodies – sucked.
The invited labs SAID, this proposal is 8%, 22%, 28%, 14%
and 15% accurate. See these statements in with own eyes in
the Dearborn booklet.
As you know I used to do method validations for Pfizer for
a living, but even the FDA will tell you your test should
detect 100% of the cases where the analyte in question is present. Certainly if there is a test that detects the closest accuracy, which is Yale’s flagellin method, would be acceptable to the FDA should this be exposed in a hearing. This method detects 94% of the cases and meets the criteria for SPECIFICITY as well not detecting flagellins from not only other pathogens, but other non-Lyme borrelia:
That being said, this Adrianna Marques of the NIH discovered that the OspA-ish or triacyl lipoproteins shed by Borrelia are responsible for the GLOBAL IMMUNOSUPPRESSION with chronic brain inflammation known to be “chronic Lyme” or post-Lyme post-sepsis syndrome:
J Neuropathol Exp Neurol. 2006 Jun;65(6):540-8.
Borrelia burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral blood monocytes but differentially regulates HLA-class II expression.
Cassiani-Ingoni R1, Cabral ES, Lünemann JD, Garza Z, Magnus T, Gelderblom H, Munson PJ, Marques A, Martin R.
Author information
1
Cellular Immunology Section, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892, USA. cassianr@ninds.nih.gov
Abstract
The spirochete Borrelia burgdorferi is the agent of Lyme disease, which causes central nervous system manifestations in up to 20% of patients. We investigated the response of human brain microglial cells, glial progenitors, neurons, astrocytes, as well as peripheral blood monocytes to stimulation with B. burgdorferi. We used oligoarrays to detect changes in the expression of genes important for shaping adaptive and innate immune responses. We found that stimulation with B. burgdorferi lysate increased the expression of Toll-like receptors (TLRs) 1 and 2 in all cell types except neurons. However, despite similarities in global gene profiles of monocytes and microglia, only microglial cells responded to the stimulation with a robust increase in HLA-DR, HLA-DQ, and also coexpressed CD11-c, a dendritic cell marker. In contrast, a large number of HLA-related molecules were repressed at both the RNA and the protein levels in stimulated monocytes, whereas secretion of IL-10 and TNF-alpha was strongly induced. These results show that signaling through TLR1/2 in response to B. burgdorferi can elicit opposite immunoregulatory effects in blood and in brain immune cells, which could play a role in the different susceptibility of these compartments to infection.
When the HLA molecules are “downregulated” that means the body is no longer going to produce antibodies or is a condition of IMMUNOSUPPRESSION.
IMMUNOSUPPRESSION is the OPPOSITE of “too many antibodies” which is the Dearborn case definition of Lyme arthritis alone.
So, that is the NIH saying the Dearborn case definition is a lie.
Marques can be subpoenaed. Martin went back home to Germany when he discovered that the MS form of Lyme was due to LYMErix like antigens causing immunosuppression… and then the reactivation of Epstein-Barr, which is mainly the cause of Multiple Sclerosis (and the others, like cancer, Lupus
and the Chronic Fatigue/post-sepsis form of Lyme).
So, like AIDS, it is the SECONDARY OPPORTUNISTICS that do all the damage.
OspA, or Pam3Cys, you can buy it, in this form, as an analog of OspA, if you want to do similar experiments discovering how they cause immunosuppression in humans:
The protein ends – Ser, Lys, Lys, Lys or whatever, are amino acids; the amino acids alone are not immunogenic, just the fatty acids (pam in pam3cys stands for palm oil, basically). As you can see in that ad to buy a Pam3Cys or OspA analog, they say it is a TLR2/1 agonist or basically FUNGAL -ish. It is sold as a congugate, as you can see with your own eyes. Fatty acids, electronegative (“sticky”) core with all those Oxygen groups and the Sulfur of Cysteine right in the middle 😀
Pam3Cys as a vaccine is like injecting bathroom scum into your bloodstream. And I am not even exaggerating.
—-
Another NIH employee, Dave Dorward, further explains how the spirochetes shed these OspA or LYMErix like antigens as, basically, THE MECHANISM of causing illness:
An NIH patent, explaining how Lyme causes LYMErix-disease:
“The invention relates to novel antigens associated with Borrelia burgdorferi which are exported (or shed) in vivo and whose detection is a means of diagnosing Lyme disease. The antigens are extracellular membrane vesicles and other bioproducts including the major extracellular protein antigen. Another object of the invention is to provide antibodies, monoclonal and/or polyclonal, labeled and/or unlabeled, that are raised against the antigens. A further object of the invention is to provide a method of diagnosing Lyme disease by detecting the antigens in a biological sample taken from a host using the antibodies in conventional immunoassay formats. Another object of the invention is to provide kits, for the diagnosis of Lyme disease, comprising the antibodies and ancillary reagents. The advantage of the antibodies used in the invention is that they react with the antigens from geographically diverse strains of Borrelia burgdorferi, but do not react with antigens from related Borrelia spirochetes.”
Did you catch that?
“The invention relates to novel antigens associated with Borrelia burgdorferi which are exported (or shed) in vivo…”
These blebs contain the Osps on them, so having Lyme disease (the real kind, where neuro outcomes are acceptable) is the same as being injected with LYMErix, or a fungal toxin.
And here is a final general statement about how Lyme is a disease of immunosuppression by a competent scientist, Nicole Baumgarth:
“Furthermore, influenza immunization administered at the time of Borrelia infection also failed to induce robust antibody responses, dramatically reducing the protective antiviral capacity of the humoral response. Collectively, these studies show that B. burgdorferi-infection results in targeted and temporary immunosuppression of the host and bring new insight into the mechanisms underlying the failure to develop long-term immunity to this emerging disease threat.”
In other words, Lyme and LYMErix cause global
immunosuppression, says the NIH.
NOT surprisingly, in I think 2012, the NIH’s Adrianna Marques said this in the New York Times, basically debunking the thugs on both sides, the CDC and ILADS (the charatans who take our last bucks for bogus treatments) said this to the New York Times:
“When Lyme Disease Lasts and Lasts” – Jane Brody, NYTimes.com
“Complicating the picture is the fact that some people with PTLDS symptoms apparently never had Lyme disease in the first place, Dr. Marques said in an interview. There are other infectious organisms — Epstein-Barr virus, for example — that can produce similar symptoms and may be the real culprits.”
IT MIGHT BE EPSTEIN-BARR!!! She says. Well known to cause chronic fatiguing mono and also the main culprit in post-sepsis syndrome. I assume you can look that up for yourself, and also find, once again, the NIH (Carolyn Beans) saying post-sepsis syndrome is about reactivated viruses like EBV (Epstein-Barr).
When the NIH says Lyme and LYMErix cause disease by immunosuppression, but the CDC says no such thing happens because they own worthless vaccine patents, well, at the very least, here are some NIH folks who can be subpoenaed to testify against the CDC criminals.
Kathleen M. Dickson
TruthCures.org and ActionLyme.org
Former Pfizer Chemist
 HERE IS THE PRESENTATION the SENATE JUDICIARY COMMITTEE and others in Washington were GIVEN, IN PERSON
https://docs.wixstatic.com/ugd/47b066_85956946d37c44d8bee5ba73d43ee5ac.pdf
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