Most of you know by now (since you’ve heard it 700 million times by TruthCures.org bloggers), that it is fairly common knowledge that in nearly all immunosuppression cases, be they transplant recipients, people exposed to Fauci’s inhalation fungi, people taking immune suppressing drugs for autoimmune diseases who are at risk for EBV-INDUCED LYMPHOMA (everyone hears this even on the TV, nearly daily in the mab commercials), or in people with dual or multiple simultaneous infections or even polymicrobial sepsis… the commonest result is the reactivation of the herpes viruses.
rOspA injections alone cause this immunosuppression/post-sepsis syndrome outcome as a fungal endotoxin with tolerance and cross tolerance to other TLR agonists besides the 1/2 which handle triacyl lipoproteins.
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You’ve heard this all along from ActionLyme and TruthCures, but we provide you the mechanisms (to the extent that they are known) and show those mechanisms in parallel – which is how science is done (The Scientific Method). In 20 years, ILADS and the non-profits of Lyme have not even made an attempt (exception, Bay Area Lyme:
Research Supported by Bay Area Lyme Foundation Shows Lower Immune Response Leads To Persistent Lyme Disease Symptoms )
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The New News from Finland (Nov 1, 2018):
“However, the research by Garg et al. argues that prolonged exposure to tick transmitted microbes weakens the human immune system increasing the host’s vulnerability to other common microbes’ labelled “non-tick-borne opportunistic microbes,” such as Chlamydia, Mycoplasma, Epstein-Barr virus and many more.”
https://www.news-medical.net/news/20181101/Tick-borne-disease-is-multiple-microbial-in-nature.aspx
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Lyme is not about spirochetes and “co-infections” as ILADS.org has been saying for 2 decades;
It, a post-sepsis syndrome outcome, is not cured by antibiotics;
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OspA injections alone cause this immunosuppression/post-sepsis syndrome outcome as a fungal endotoxin with tolerance and cross tolerance to other TLR agonists besides the 1/2 which handle triacyl lipoproteins (see the TruthCures.org or ActionLyme.org “Criminal Charges Sheets” – which are criminal charges since this, the Lyme crimes, all revolve around tossing out this very immunosuppression disease at Dearborn to pass off this bogus OspA Lyme vaccines by the CDC staff who owned patents and their co-corrupt-cronies at Yale.edu and NYMC.edu – the ALDF.com);
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This is what we have come up with so far. Feel free to do your own research:
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(1)…. MECHANISMS by which OspA reactivate latent herpes (IL-10 & Mario Philipp, vIL-10 means the EBV virus’ own version of it):
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The EBV Immunoevasins vIL-10 and BNLF2a Protect Newly Infected B Cells from Immune Recognition and Elimination
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“vIL-10 impairs NK cell mediated killing of infected B cells, interferes with CD4+ T-cell activity, and modulates cytokine responses, while BNLF2a reduces antigen presentation and recognition of newly infected cells by EBV-specific CD8+ T cells. Together, both factors significantly diminish the immunogenicity of EBV-infected cells during the initial, pre-latent phase of infection and may improve the establishment of a latent EBV infection in vivo.”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3355093/
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Mario Philipp, OspA and the induction of the immunosuppressive cytokine IL-10:
https://www.ncbi.nlm.nih.gov/pubmed/?term=Philipp+and+IL-10+and+OspA
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Recall that I mentioned this, as well as the issue with Dattwyler’s “inert NK cells in the presence of Borrelial fatty acid supernatant reports” when I blew the whistle at the FDA in Jan 2001 on this, OspA causing immunosuppression – and that the Dearborn criteria was not a consensus at this “consensus” conference.
https://web.archive.org/web/20040203184937/http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_11.pdf
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Dattwyler from 1988
Modulation of Natural Killer Cell Activity by Borrelia burgdorferia
First published: August 1988
https://nyaspubs.onlinelibrary.wiley.com/doi/abs/10.1111/j.1749-6632.1988.tb31843.x
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http://www.actionlyme.org/DATTWYLER_NK_SUPPRESSION.htm << Full Text
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Continuing (2)…. MECHANISMS by which OspA reactivate latent herpes… (few things are better than a fungal triacyl Osp for activating EBV; this one is about how OspA *IS* very clearly associated with the reactivation of EBV better than “normal” sepsis inducers like whatever is a non-spirochete):
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Few things are better than LYMErix/OspA for activating Epstein-Barr:
https://crymedisease.wordpress.com/2018/11/06/few-things-are-better-than-lymerix/
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Toll-Like Receptor Agonists [PAM3CYS – see the article] Synergistically Increase Proliferation and Activation of B Cells by Epstein-Barr Virus ▿
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2838115/
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Continuing (3)…. MECHANISMS by which OspA reactivate latent herpes… (Inhibiting APOPTOSIS; both EBV and OspA do it):
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“INHIBITION OF APOPTOSIS…” “Stealth bomber” spirochetes shed highly acylated TLR2/1 agonists, turning off the immune system, AKA “Post-Sepsis Syndrome.”
https://crymedisease.wordpress.com/2016/08/02/inhibition-of-apoptosis/
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Continuing (4)…. MECHANISMS by which OspA reactivate latent herpes… (causes tolerance to other TLR agonists types besides TLR2/1 – Harding and Boom):
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Mycobacterium tuberculosis and TLR2 agonists inhibit induction of type I IFN and class I MHC antigen cross processing by TLR9.
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“Dendritic cells (DCs) cross process exogenous Ags and present them by class I MHC (MHC-I) molecules to CD8(+) T cells specific for Ags from viruses and bacteria such as Mycobacterium tuberculosis. Unmethylated CpG DNA signals through TLR9 to induce type I IFN (IFN-alpha/beta), which enhances MHC-I Ag cross processing, but lipoproteins that signal through TLR2 do not induce IFN-alpha/beta. In these studies we observed that M. tuberculosis, which expresses agonists of both TLR9 and TLR2, did not induce production of IFN-alpha/beta or cross processing by murine DCs. Furthermore, M. tuberculosis and TLR2 agonists inhibited induction of IFN-alpha/beta and DC cross processing by CpG DNA. Exogenous IFN-alpha/beta effectively enhanced cross processing of M. bovis bacillus Calmette-Guérin expressing OVA, bypassing the inhibition of induction of endogenous IFN-alpha/beta. In addition, inhibition of TLR9-induced cross processing of M. bovis bacillus Calmette-Guérin expressing OVA could be circumvented by pretreating cells with CpG DNA to induce IFN-alpha/beta and MHC-I cross processing before inhibitory mycobacterial TLR2 agonists were present. Inhibition of the response to one TLR by another may affect the ultimate response to pathogens like M. tuberculosis that express agonists of multiple TLRs, including TLR2 and TLR9. This mechanism may contribute to immune evasion and explain why IFN-alpha/beta provides little contribution to host immunity to M. tuberculosis. However, downregulation of certain TLR responses may benefit the host by preventing detrimental excessive inflammation that may occur in the presence of persistent infection.”
https://www.ncbi.nlm.nih.gov/pubmed/20660347
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Continuing (4a) … MECHANISMS by which Borrelia and their shed Osps help activate EBV et al. This would be a continuation or an addition to the Harding claim that lipoproteins cause cross tolerance the the TLRs that handle viruses, which was also SHOWN by Baumgarth when exposing Lyme-ridden mice to an influenza virus:
Toll-like receptor 7 is required for effective adaptive immune responses that prevent persistent virus infection
“Chronic viral infections such as human immunodeficiency virus, hepatitis B virus and hepatitis C virus (HCV) result in dysfunctional immune responses, including altered innate immune responses, T cell exhaustion and defective B cell responses (Frebel et al., 2010; Liu et al., 2009; Oliviero et al., 2011; Urbani et al., 2006). Understanding the mechanisms that cause viral persistence should lead to optimally planned therapies to overcome such infections. For example, the subversion of host T and B cell immune responses through up-regulation of host negative immune regulators (NIRs) effectively exacerbated persistence and blockade of NIR signaling such as IL-10, PD-1, TGF-β, and LAG-3 resurrected T cell function that enhanced viral clearance and terminated the persistent infection (Barber et al., 2006; Blackburn et al., 2009; Brooks et al., 2006; Tinoco et al., 2009).”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3377981/
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Continuing (5)…. MECHANISMS by which OspA reactivate latent herpes… (downregulates antigen presentation- with the cross tolerance to other TLR agonists- SAYS THE NIH!!!):
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Borrelia burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral blood monocytes but differentially regulates HLA-class II expression.
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“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.”
https://www.ncbi.nlm.nih.gov/pubmed/16783164
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Continuing (6)…. MECHANISMS by which OspA reactivate latent herpes… (Could the downregulation of those HLAs by the Osps be associated with the reactivation of EBV ? from 2002)
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The lytic cycle of Epstein-Barr virus is associated with decreased expression of cell surface major histocompatibility complex class I and class II molecules.
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“Using two-color immunofluorescence staining of cell surface antigens and EBV-encoded lytic cycle antigens, we examined EBV-transformed B-cell lines in which a small subpopulation of cells had spontaneously entered the lytic cycle. Cells in the lytic cycle showed a four- to fivefold decrease in cell surface expression of MHC class I molecules relative to that in latently infected cells. Expression of MHC class II molecules, CD40, and CD54 was reduced by 40 to 50% on cells in the lytic cycle, while no decrease was observed in cell surface expression of CD19, CD80, and CD86. Downregulation of MHC class I expression was found to be an early-lytic-cycle event, since it was observed when progress through late lytic cycle was blocked by treatment with acyclovir.”
https://www.ncbi.nlm.nih.gov/pubmed/12134023
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Contining (7) … THIS IS NOT A MECHANSIM but an observation that we dont have the full text of, and no one cited it in their subsequent reports. Hulinska. What’s different about garinii
Folia Biol (Praha). 2003;49(1):40-8.
Interaction of Borrelia burgdorferi sensu lato with Epstein-Barr virus in lymphoblastoid cells.
Hulínská D1, Roubalová K, Schramlová J.
Author information
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National Reference Laboratory on Borreliosis, Electron Microscopy, National Institute of Public Health, Prague, Czech Republic.
Abstract
Since the possibility of interruption of latent EBV infection has been suggested by the induction of the lytic virus cycle with chemical substances, other viruses, and by immunosuppression, we hypothesized that the same effect might happen in B. burgdorferi sensu lato infection as happens in Lyme disease patients with positive serology for both agents. We have observed EBV replication in lymphoblastoid cells after superinfection with B. garinii and B. afzelii strains after 1 and 4 h of their interaction. We found that viral and borrelial antigens persisted in the lymphoblasts for 3 and 4 days. Morphological and functional transformation of both agents facilitate their transfer to daughter cells. ****Association with lymphoblasts and internalization of B. garinii by tube phagocytosis increased replication of viruses more successfully than B. afzelii and chemical inductors.**** Demonstration of such findings must be interpreted cautiously, but may prove a mixed borrelial and viral cause of severe neurological disease.
https://www.ncbi.nlm.nih.gov/pubmed/12630667
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Continuing (8) MECHANISMS BY WHICH THE OSPS ACTIVATE EBV… This is sorta new and interesting about the B cells in the CSF being **abnormally associated** with spirochetes….(B cells harbor both EBV and spirochetes as do lymph nodes and bone marrow). I am looking for why garinii would be better at activating EBV than the other B-chetes….
****This report says it is definitely the likes of LYMErix causing the brain inflammation,*** although that’s not what we are looking for right now. We are looking for the mechanisms for how Lyme activates EBV (besides the fact that that usually happens in all other immunosuppression cases; we still would like to know exactly how and why, especially with a new OspA vaccine with pam3cys on it, on the horizon).
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Borrelia garinii Induces CXCL13 Production in Human Monocytes through Toll-Like Receptor 2▿
“After crossing the blood-brain barrier, both spirochetes elicit an inflammatory response in the cerebrospinal fluid (CSF), predominantly mediated by mononuclear cells. This contrasts with the massive invasion of polymorphonuclear cells into the CSF of patients with pneumococcal meningitis (PM), the most frequent bacterial infection of the adult CNS. …
“B lymphocytes, in contrast to other leukocytes, show substantial migration in response to only a very few chemokines, namely, CCL19, CCL21, CXCL12, and CXCL13 (3). Since the proportion of B lymphocytes in the CSF infiltrate in NB patients is higher than the proportion resulting from any other CNS infection (6), the chemokines listed above might play an important role in NB-induced inflammatory CNS reactions. …
[remembering that the opposite occurs in the peripheral blood – low to no signs of inflammation or antibodies]
“Recently, we demonstrated presence of CXCL13 in the CSF of patients with NB at high levels (19).”
“Accordingly, we found that the lipid moiety N-palmitoyl-S-(bis[palmitoyloxy]propyl)cystein (Pam3C) (three palmitoyl residues bound to N-terminal cysteine) of the spirochetal lipoproteins is critical for the CXCL13 induction in monocytes.”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1951179/
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They simply might have more of the triacyl Osps since I am pretty sure garinii infects more species. May have to do with the OspCs (ligands for something on RBCs):
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Continuing (9)…. MECHANISMS by which OspA reactivate latent herpes… This one is about TLR2 handing some surface proteins of EBV, which, we know the Osps tolerize against TLR2 agonists and render them inert; so this could be a real, contributing mechanism:
Exploiting the Interplay between Innate and Adaptive Immunity to Improve Immunotherapeutic Strategies for Epstein-Barr-Virus-Driven Disorders
“TLR2 was reported to recognize several PAMPs conserved on virions from different members of human herpesviruses. TLR9 is an important receptor for nucleic-acid-containing unmethylated CpG motifs present in both bacterial and viral DNA, whereas TLR7 senses single-stranded RNA [130]. A rapid detection of EBV particles during primary infection and the detection of secreted components or reactivated virus from EBV-infected cells are crucial for an efficient control of EBV infection. Intact viral particles are recognized by the membrane surface TLR2 (Figure 1) [131], likely through the interaction with gp350, the major envelope glycoprotein which mediates also EBV entry into B cells [132]. In addition, TLR2 is involved in the recognition of the unstructural protein dUTPase, which determines the activation of NF-κ B via MyD88-dependent signalling cascade and induces expression of proinflammatory cytokines in macrophages [133]. Following viral entry into the cells, viral DNA is subsequently recognized by TLR9 (Figure 1). Such dual interactions, through TLR2 on cell membrane and by intracellular TLR9, lead to a rapid production of IL-8 to initiate an effective immune response. Production of MCP-1 and IL-10 by monocytes in response to EBV is mainly dependent on TLR2 rather than TLR9 [134]. Therefore, because monocytes express low levels of TLR9, it seems plausible that they have acquired the ability to use one TLR, in this case TLR2, to produce different cytokines to better respond to EBV before its entry into the cell.”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3272797/
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Cryme Disease - Unscrambling the CDC's DNA Patent Profiteering Bullshit 