THE COUNT… waiting for ILADS, Day 10

THE COUNT, Day 10 (Nov 10, 2018):
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Waiting for ILADS.org and the fake non-profits to admit TC/AL* was right, that Lyme and LYMErix diseases (LLDs) were really about the reactivated viruses and that LLD was a form of post-sepsis syndrome.

ILADS and the LDA/LDo still have not mentioned the fact that Lyme causes chronic abx-incurable illness by activating EBV

et al,

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“Evidence from mouse and human studies indicate that pathogenesis by various tick-borne associated microbes15,16,17 may cause immune dysfunction and alter, enhance the severity, or suppress the course of infection due to the increased microbial burden18,19,20,21,22. As a consequence of extensive exposure to tick-borne infections15,16,17, patients may develop a weakened immune system22,23, and present evidence of opportunistic infections such as Chlamydia spp.24,25,26,27, Coxsackievirus28, Cytomegalovirus29, Epstein-Barr virus27,29, Human parvovirus B1924, and Mycoplasma spp.30,31. “
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^^  That’s pretty clear and succinct, if you ask me.  Antibiotics dont cure immunosuppression, tolerance and cross tolerance to fungal antigens (shed triacyl lipoproteins of Borreliae) or reactivated viruses, or the tissue damage known to occur from polymicrobial sepsis.  ‘Which is the same thing as LLDs.  Neither do “supplements” or “immune boosters.”

Whoever offers these as a “treatment” should provide the scientific substantiation from the journals as to how these supplements work, exactly.

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despite the fact that the NIH and Yale had “Lyme and MS,” and “Lyme and Lupus” Clinics (when those are both known to be caused by the herpesviruses).

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Here is the former manager of the Yale “Lyme and Lupus Clinic,” Joe Craft:

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J Immunol. 2004 Jan 15;172(2):1287-94.
Defective control of latent Epstein-Barr virus infection in systemic lupus erythematosus.
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Kang I1, Quan T, Nolasco H, Park SH, Hong MS, Crouch J, Pamer EG, Howe JG, Craft J.
Author information
Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, 300 Cedar Street, New Haven, CT 06520, USA.
Abstract
EBV infection is more common in patients with systemic lupus erythematosus (SLE) than in control subjects, suggesting that this virus plays an etiologic role in disease and/or that patients with lupus have impaired EBV-specific immune responses. In the current report we assessed immune responsiveness to EBV in patients with SLE and healthy controls, determining virus-specific T cell responses and EBV viral loads using whole blood recall assays, HLA-A2 tetramers, and real-time quantitative PCR. Patients with SLE had an approximately 40-fold increase in EBV viral loads compared with controls, a finding not explained by disease activity or immunosuppressive medications. The frequency of EBV-specific CD69+ CD4+ T cells producing IFN-gamma was higher in patients with SLE than in controls. By contrast, the frequency of EBV-specific CD69+ CD8+ T cells producing IFN-gamma in patients with SLE appeared lower than that in healthy controls, although this difference was not statistically significant. These findings suggest a role for CD4+ T cells in controlling, and a possible defect in CD8+ T cells in regulating, increased viral loads in lupus. These ideas were supported by correlations between viral loads and EBV-specific T cell responses in lupus patients. EBV viral loads were inversely correlated with the frequency of EBV-specific CD69+ CD4+ T cells producing IFN-gamma and were positively correlated with the frequencies of CD69+ CD8+ T cells producing IFN-gamma and with EBV-specific, HLA-A2 tetramer-positive CD8+ T cells. These results demonstrate that patients with SLE have defective control of latent EBV infection that probably stems from altered T cell responses against EBV.
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Here is Allen Steere talking about how Lyme causes Lupus:

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J Neurol Sci. 1993 Jul;117(1-2):206-14.
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Reactivity of neuroborreliosis patients (Lyme disease) to cardiolipin and gangliosides.
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García Moncó JC1, Wheeler CM, Benach JL, Furie RA, Lukehart SA, Stanek G, Steere AC.
Author information
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Department of Pathology, SUNY, Stony Brook 11794.
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Abstract
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A subset of patients (50%) with neuroborreliosis (Lyme disease) showed IgG reactivity to cardiolipin in solid phase ELISA. In addition, a subset of patients with neuroborreliosis (29%) and syphilis (59%) had IgM reactivity to gangliosides with a Gal(beta 1-3) GalNac terminal sequence (GM1, GD1b, and asialo GM1). Anti-ganglioside IgM antibodies were significantly more frequent in these two groups of patients compared to patients with cutaneous and articular Lyme disease, primary antiphospholipid syndrome, systemic lupus erythematosus and normal controls. Correlative evidence and adsorption experiments indicated that antibodies to cardiolipin had separate specificities from those directed against the gangliosides. IgM antibodies to Gal(beta 1-3) GalNac gangliosides appeared to have similar specificities since these were positively correlated and inhibitable by cross adsorption assays. Given the clinical associations of patients with neuroborreliosis and syphilis with IgM reactivity to gangliosides sharing the Gal(beta 1-3) GalNac terminus, we suggest that these antibodies could represent a response to injury in neurological disease or a cross reactive event caused by spirochetes.

And ^^^ that was after Steere said Lyme caused post-sepsis syndrome with the reactivated EBV et al with Paul Duray, in 1988.  And around the same time Steere THREW OUT all those IgM bands when he falsified the case definition for Dearborn by introducing the high-cut off ELISA:

 

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Ann N Y Acad Sci. 1988;539:65-79.
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Clinical pathologic correlations of Lyme disease by stage.
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Duray PH1, Steere AC.
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Author information
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Department of Pathology, Fox Chase Cancer Center, Philadelphia, Pennsylvania 19111.
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Abstract
Lyme disease is capable of producing a wide variety of clinical pathologic conditions and lesions having in common histologic features of collagen-vascular disease. The plasma cell is an omnipotent inflammatory responder in most tissues involved by Lyme disease, ranging from relatively acute to lesions that have gone on for years. Vascular thickening also seems to be prominent, and in the dermis is accompanied by scleroderma-like collagen expansion. The disease in some ways resembles the responses seen in lupus erythematosus such as mild cerebritis with lymphocytes and plasma cells in the leptomeninges. Lymphoplasmacytic panniculitis of Lyme disease resembles lupus profundus, both in the infiltrate and the plasma cell-blood vessel relationship. The onion skin thickened vessels of the synovia resemble the vessels of lupus spleens, while the scleradermoid thickening of the dermis and various skin lesions of stage III Lyme disease suggest a collagen-vascular disorder. Finally, the perivascular lymphoid infiltrate in clinical myositis does not differ from that seen in polymyositis or dermatomyositis. All of these histologic derangements suggest immunologic damage in response to persistence of the spirochete, however few in number.
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“Histologic Derangements.”
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Just like sepsis.
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Here is the full text of that if you want the relatively grotesque details:
http://www.actionlyme.org/clinical-pathologic-correlations-of-lyme-disease-by-stage-Steere-Duray.pdf
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Now think.  WHO has been telling you about how Lyme and LYMErix disease is about the reactivated viral infections since the Osps are fungal (pam3cys) or triacylated, cause tolerance and cross tolerance, and are classic activators of latent infections…??
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And who also knew, but remained silent for over 15 years?
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Yep, you guessed it.  The group that became ILADS.
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*TC/AL = Truthcures.org and ActionLyme.org, which are now the same group, TruthCures.org
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