Where are all the scientists who say Lyme and LYMErix (Pam3Cys) are diseases of generalized immunosuppression, are really “Post Sepsis Syndrome,” (are about reactivated latent viruses like the herpes and not really about spirochetes or biofilms) and with chronic brain inflammation??
Of course, everyone knows these real scientists are not in ILADS.org or except in one instance (see below) are ever considered “LLMDs.” The “LLMDs” all tell you they can cure you.
The non-nonprofits (“nons”) want you to talk about your personal case (“BigData?” LMAO), not knowing anecdotal, subjective testimony is not valid data.
ILADS and the nons insist they will never talk about how the CDC’s “case definition” for Lyme was falsified at Dearborn (1994) such as to say “Lyme is ONLY an inflammatory- HLA-linked-, autoimmune disease.”
ILADS and the nons have also sworn never to explain what OspA is, or how it caused the same immunosuppression/AIDS like disease as Chronic Neurologic Lyme itself.
They said this stance is due to the fact that they “refuse to be helping Kathleen Dickson get the qui tam / whistleblower / False Claims Act money,” completely unaware that if any information in the claim is publicly known, no one gets the qui tam money. The ILADS/nons gang does not even know the law on this and they have (Hollywood actors’) “lawyers” in their camp!
ILADS and the nons do not know how to argue this crime, yet there are supposedly “doctors” and “lawyers” among them. Half of their problem is that they choose not argue scientifically or correctly or expose the conflicts of interest because that would be the end of their $$$ gravy trains.
Think: What would happen if tomorrow the CDC caved and admitted they lied about “Lyme disease,” that indeed, it is just another relapsing fever organism, and that OspA-ish antigens shed by borrelia on blebs causes the chronic B cell disorder also known as post-sepsis syndrome (look that up). WHO would immediately not be raking in 100s of thousands of dollars a year to do NOTHING effective?
Panas, from Harvard, where they are hiding Allen Steere in his “high-security” T cell freezers from us Lyme activists and lobbyists who are in Albany, trying to get that asshole thrown in jail:
Go ahead and check those references 7-10 below (Harding):
“Slow-growing mycobacteria, including Mycobacterium tuberculosis and Mycobacterium bovis, have evolved mechanisms to evade host immune responses. These mycobacteria have been shown to alter vesicle trafficking and acidification, allowing them to survive for extended periods of time in the phagocytic compartments of macrophages (1,–3). They evade host cellular immune responses by modulating type I interferon production (4, 5) and inhibit apoptosis of infected macrophages (6). A number of studies have shown that these mycobacteria can inhibit major histocompatibility complex (MHC) class II-restricted peptide presentation (7,–10). It has also been suggested that mycobacteria may be capable of evading MHC class I-restricted T cell responses, but the mechanisms mycobacteria utilize to do so have not yet been defined.”
This author ^^, Panas, says fungal antigens like LYMErix cause immunosuppression, and is also a signer of the new, Non-Dearborn, semi-valid test, put out by Dattwyler, Steere and Aucott, debunking all the “if it is not a bad knee, it must not be Lyme,” fraud, slander and libel by the CDC Lyme crooks. People wondered, was there a tie-in between the scientists who say Tb fungal antigens cause immunosuppression, like Hotchkiss, Baumgarth, Radolf, Medvedev, and Harding and the ones who say OspA is also such a TLR2/TLR1 agonist that ALSO causes immunosuppression? There is your man. Harvard. I guess Harvard finally gets a mental competency award of some sort.
Who else, then, besides Panas at Harvard, who says Borreliosis or shed OspA-ish fungal antigens (tlr2/1-agonists) cause systemic immunosuppression, post-sepsis, and with a chronically inflamed brain?
Don’t you think you are entitled to know ILADS and the nons are clueless and ought not to be anywhere near Lyme victims?
Baumgarth, & Barthold, UCal, Davis:
UCSF also says Lyme and LYMErix-Disease are a diseases of immunosuppression, and they say that half the Lyme/tick bite victims remain ill and are not cured with antibiotics
Feb 12, 2016:
“Early Lyme disease prior to antibiotic therapy was characterized by marked upregulation of Toll-like receptor signaling but lack of activation of the inflammatory T-cell apoptotic and B-cell developmental pathways seen in other acute infectious syndromes,” wrote the study’s authors. “Six months after completion of therapy, Lyme disease patients were found to have 31 to 60% of their pathways in common with three different immune-mediated chronic diseases. No differential gene expression signature was observed between Lyme disease patients with resolved illness to those with persistent symptoms at six months post-treatment.”
Clifford Harding (Case Western Reserve) and Justin Radolf (UConn):
Andrei Medvedev, University of Maryland, Baltimore and now UConn:
Induction of in vitro reprogramming by Toll-like receptor (TLR)2 and TLR4 agonists in murine macrophages: effects of TLR “homotolerance” versus “heterotolerance” on NF-kappa B signaling pathway components.
Redmond, National University of Ireland:
These people straight up say “Chronic Lyme” is really about immunosuppression and the reactivation of latent herpes viruses. The same thing happens post-sepsis. OspA carried around on shed blebs inflame the brain and cause generalized immunosuppression, identical to post-sepsis.
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.” [OspA]
Hotchkiss and the NIH, Washington University, St. Louis:
Exposure to the likes of OspA causes immunosuppression and the reactivation of various herpesviruses. It seems clear to me the NIH knew it since the late 1980s since Paul Duray worked for the NIH and also published in IDSociety.org’s very journal about how exposure to Lyme seems to reactivate Epstein-Barr.
Mario Philipp, Tulane:
Diego Cadavid on OspA on the blebs getting into the brain to inflame it, which is the same as what the NIH says (Martin and Marques):
Bacterial lipoproteins can disseminate from the periphery to inflame the brain.
“The current view is that bacteria need to enter the brain to cause inflammation. However, in mice infected with the spirochete Borrelia turicatae, we observed widespread cerebral inflammation despite a paucity of spirochetes in the brain parenchyma at times of high bacteremia. Here we studied the possibility that bacterial lipoproteins may be capable of disseminating from the periphery across the blood-brain barrier to inflame the brain. For this we injected normal and infected mice intraperitoneally with lanthanide-labeled variable outer membrane lipoproteins of B. turicatae and measured their localization in blood, various peripheral organs, and whole and capillary-depleted brain protein extracts at various times. Lanthanide-labeled nonlipidated lipoproteins of B. turicatae and mouse albumin were used as controls. Brain inflammation was measured by TaqMan RT-PCR amplification of genes known to be up-regulated in response to borrelial infection. The results showed that the two lipoproteins we studied, LVsp1 and LVsp2, were capable of inflaming the brain after intraperitoneal injection to different degrees: LVsp1 was better than LVsp2 and Bt1 spirochetes at moving from blood to brain. The dissemination of LVsp1 from the periphery to the brain occurred under normal conditions and significantly increased with infection. In contrast, LVsp2 disseminated better to peripheral organs. We conclude that some bacterial lipoproteins can disseminate from the periphery to inflame the brain.”
More by Cadavid on Borrelia and the brain:
Gary Wormser, Ira Schwartz, New York Medical College:
Modulation of lymphocyte proliferative responses by a canine Lyme disease vaccine of recombinant outer surface protein A (OspA).
“The modulation of human lymphocyte proliferative responses was demonstrated with a recombinant outer surface protein A (OspA) vaccine preparation for the prevention of Borrelia burgdorferi infection. After exposure to either the unaltered vaccine preparation or OspA prepared in saline, normal lymphocyte responses to the mitogens concanavalin A, phytohemagglutinin-M or pokeweed mitogen, or the antigen BCG were consistently reduced. Whole cell extracts of B. burgdorferi also modulated immune responses but required a much greater quantity of protein than needed for theOspA 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 theOspA molecule responsible for this effect may lead to improved vaccine preparations.”
Kenneth B. Liegner, private practice, Critical Care Medicine, trained at McGill:
Antigens of Lyme disease of spirochaete Borrelia burgdorferi inhibits antigen or mitogen-induced lymphocyteproliferation.
“Modulation of cellular immune responses by the spirochaete Borrelia burgdorferi, the bacteria that causes Lyme disease, was demonstrated. When cultured in the presence of sonicated Borrelia preparation (Bb), the mitogen- or antigen-stimulated proliferative responses of normal lymphocyteswere consistently lowered. Bb caused the greatest reduction in Concanavalin A (ConA) or antigen-stimulated proliferation, where almost 100% reduction in proliferation could be achieved. Bb also reduced phytohemagglutinin-M (PHA) or pokeweed mitogen (PWM)-stimulated peripheral bloodlymphocyte (PBL) proliferation, with the PWM proliferation being the least affected. This regulatory activity was not due to toxicity and was determined to be caused by Bb protein antigens. The degree of the proliferation reduction was directly proportional to both Bb quantity and length of exposure tolymphocytes. IL-2 production was significantly reduced from Bb-exposed lymphocytes. The entry of lymphocytes into the proliferating phases of the cell cycle was also shown to be blocked. These results have demonstrated an immune suppressive mechanism of B. burgdorferi. The magnitude of host immune responses may be dependent on the degree of suppression which is related to the spirochaete quantity and their length of presence in the host.”
Baumgarth and Barthold (UCDavis)