You need a
graphic or two. This one shows the
shed blebs or exosomes.
They have LYMErix on them which is
how Lyme causes disease - by shedding
fungal blebs that turn off the immune
response, it is like a slow sepsis; Yale
wanted to inject everyone with these.
They go right to your brain and cause
brain damage, as you will see....
1) MARCH 2002: Organisation of the pericentromeric region of chromosome 15: at least four partial gene copies are amplified in patients with a proximal duplication of 15q.
"We identified a fourth pseudogene, BCL8A [a BCL-2 class molecule, which inhibits apoptosis is reverse-duplicated and therefore overexpressed- KMD], which maps to the pericentromeric region and is coamplified along with the NF1 sequences. Interphase FISH ordering experiments show that IgH D lies closest to the centromere, while BCL8A is the most distal locus in this pseudogene array;" http://www.ncbi.nlm.nih.gov/pubmed/11897815
Reversed duplications imply the anti-apoptosis gene is probably over-expressed. The New York Times recently (summer, 2014) ran an article about another mechanism of inhibition of apoptosis leading to the genetic kind of autism, as if that was news, given what we know about the co-occurance of Einstein kind of Autism in Neurofibromatosis. This connection was written up in all the older books on “psychiatry,” duh.
Update, NYT, Aug 2014:
Study Finds That Brains With Autism Fail to Trim Synapses as They Develop
And is associated with Neurofibromatosis- 1
2) – BigPharma: Patent, US # 7,632,510
Methods of inducing flavivirus immune responses through the administration of recombinant flaviviruses comprising an engineered japanese encephalitis virus signal sequence
"Finally, there is the risk that the virus may not be fully or completely inactivated or attenuated and thus, the vaccine may actually cause disease."
3) CDC: Measles, Mumps, and Rubella -- Vaccine Use and Strategies for Elimination of Measles, Rubella, and Congenital Rubella Syndrome and Control of Mumps: Recommendations of the Advisory Committee on Immunization Practices (ACIP)
"Updated information on adverse events and contraindications, particularly for persons with severe HIV infection, persons with a egg allergy or gelatin allergy, persons with a history of thrombocytopenia, and persons receiving steroid therapy [are immunosuppressed - KMD]."
IDSA admits vaccines not safe for babies
“Amanda Jezek, the vice
president of Public Policy and Government Relations at the Infectious
Diseases Society of America (IDSA), in Arlington, Va., said there is
concern that this push to recommend a vaccine before the ACIP has
reviewed the evidence would completely “jeopardize the integrity of
Fauci just announced (Sep, 2014) huge new funding for adjuvants for vaccines for immunosuppressed children, duh, why would he do that if this was not a problem.
"NIH awards seven new vaccine adjuvant discovery contracts"
"The goal of this research is to identify novel adjuvant candidates that safely and selectively boost vaccine-induced immune responses,” said NIAID Director Anthony S. Fauci, M.D. “Such adjuvants could be used to improve current vaccines, extend the vaccine supply or enhance vaccine efficacy in people with immature or weakened immune systems, such as infants and the elderly.”
4) CDC: Human Exposure to Brucella abortus Strain RB51 -- Kansas, 1997
In the above, an immunosuppressed pregnant cow was given a Brucella (“LYME”rix-like) "live attenuated" vaccine and the baby cow ended up with the disease, which then was transferred to the humans handling the cow and her dead baby. This parallels what is happening to children who are vaccinated while immunosuppressed, or who receive mycoplasmally (“LYME”rix-like) contaminated vaccines.
5) In the case of pandemic MRSA, as we have seen, the vaccine didn't work because TLR2 agonists (lipoproteins) suppress the immune system. We also learned from the MRSA vaccine patent, that (US patent 7,771,728)
Method for identification, isolation and production of antigens to a specific pathogen
"Several established vaccines consist of live attenuated organisms where the risk of reversion to the virulent wild-type strain exists. In particular in immunocompromised hosts this can be a live threatening scenario. Alternatively, vaccines are administered as a combination of pathogen-derived antigens together with compounds that induce or enhance immune responses against these antigens (these compounds are commonly termed adjuvant), since these subunit vaccines on their own are generally not effective."
6) The effect of exogenous corticosterone on West Nile virus infection in Northern Cardinals (Cardinalis cardinalis)
“Corticosterone was administered at levels that individuals enduring chronic stressors (i.e ., long-term inclement weather, food shortage, anthropogenic pollution) might experience in the wild. Corticosterone greatly impacted mortality: half of the corticosterone-implanted cardinals died between five - 11 days post-inoculation whereas only one of nine sham-implanted (control) birds died.
”No differences were found in viral titer between corticosterone- and sham-implanted birds. However, cardinals that survived infections had significantly higher average body temperatures during peak infection than individuals that died.
”In sum, this study indicates that elevated corticosterone could affect the survival of WNV-infected wild birds, suggesting that populations may be disproportionately at-risk to disease in stressful environments.”
The same is true for humans and cortisol and the activation of latent herpesviruses, therefore it’s not “psychiatric” or “psychosomatic,” it’s EBV due to cortisol, meaning real and not due to having the powers of a witch. (Later we add this data, in this project, and you can see it now in the next section.)
7) NYTimes; Doctors admit Thimerosal is put in vaccines to prevent fungi:
Vaccine Rule Is Said to Hurt Health Efforts (Dec, 2012)
"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.'"
^^ They are revealing why so few doctors' own kids get vaccines-acquired brain damage. Their kids probably get the first shot out of the vial.
8) Fungi Activate Viruses, Rockefeller, 1953 [Go back to the 1950s to see Rockefeller Bioweapons Inc experimenting with mycoplasma antigens like OspA - Enhancing Mouse Leukemia Virus, just like fungally-contaminated vaccines do, which was the reason they put Thimerosal in vaccines, to prevent fungi from doing this (Clue: HIV and "Lyme" bearing the same immunosuppressing triacyl lipopeptide fungal antigen, OspA]:
ACUTE HEPATITIS ASSOCIATED WITH MOUSE LEUKEMIA
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 and the virus component of Gledhill, Dick, and Andrewes, which is nearly inactive when injected alone, resulted in acute hepatitis with fatal outcome."
9) OspA acts like BCL2, inhibiting apoptosis reactivating EBV/Similars:
Targeting proteins computationally
"Apoptosis is regulated by both pro- and anti-apoptotic members of the B cell lymphoma-2 (Bcl-2) family of proteins. Epstein Barr virus (EBV), the causative agent of Burkitt’s lymphoma, encodes a pro-survival mimic of these Bcl-2 proteins called BHRF1 that inhibits cellular apoptosis during infection and is thought to contribute to lymphomagenesis."
10) This is the NIH (NINDS’s MS-Lyme Group) group that discovered that *** OspA *** was the cause of the MS/New Great Imitator outcome of Lyme reporting in the New York Times in the summer of 2013 (Martin and Marques, 2006):
When Lyme Disease Lasts and Lasts – Jane Brody
"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."
Here are the NIH's 2 reports that say OspA (TLR2-agonist) is the cause of the MS/CFIDS/EBV-reactivated kind of Lyme (that also causes humoral immunosuppression),... and that as a result of exposure to OspA-like antigens (shed constantly in a process called blebbing, as revealed by CDC officer Alan "Stealth Bomber" Barbour), you might not even have anti-flagellar antibodies (TLR5-agonists):
Borrelia burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral blood monocytes but differentially regulates HLA-class II expression.
Borrelia burgdorferi lipoprotein-mediated TLR2 stimulation causes the down-regulation of TLR5 in human monocytes.
11) Wustl.edu discover (?- wow, thanks) that sepsis is lyke Lyme, in that the survivors of it are likely to have survived via the immunosuppression (TLR2-agonist tolerance/Endotoxin tolerance), but the result is the reactivation of latent viruses:
Dormant viruses re-emerge in patients with lingering sepsis, signaling immune suppression
"Patients with lingering sepsis had markedly higher levels of viruses detectable in the blood, compared with the healthy controls and critically ill patients without sepsis. Among the sepsis patients, for example, the researchers found that 53 percent had Epstein-Barr virus, 24 percent had cytomegalovirus, 14 percent had herpes-simplex virus, and 10 percent had human herpes simplex virus-7.
"These viruses generally don’t lead to significant illness in people who are healthy but can cause problems in patients who are immune-suppressed. "
FULL JOURNAL REPORT, snippet…
Reactivation of Multiple Viruses in Patients with Sepsis
“Sepsis is the host's non-resolving inflammatory response to infection that leads to organ dysfunction , . A current controversial hypothesis postulates that if sepsis pursues a protracted course, it progresses from an initial primarily hyper-inflammatory phase to a predominantly immunosuppressive state –. Experimental therapeutic approaches in sepsis have almost exclusively focused on blocking early inflammation or host-pathogen interaction and failed –. Recently, immuno-adjuvant therapies that boost host immunity, e.g., GM-CSF and interferon-γ, have been successful in small clinical trials thereby supporting the concept that reversing immunosuppression in sepsis is a plausible strategy to improve outcome , . However, several issues have limited this approach including lack of consensus that immunosuppression is a clinically important phenomenon , , . Also, difficulty in identifying patients with impaired immunity as well as determining optimal timing for administration pose significant challenges to pursuing this approach . While immuno-adjuvant therapies might improve sepsis survival if administered during the later immunosuppressive phase, these agents might worsen outcome if given during the early hyper-inflammatory phase , . Thus, a means to distinguish these two contrasting phases of sepsis is needed not only to verify the hypothesis that sepsis progresses to an immunosuppressive state but also to guide use of potential agents which boost immunity.
“Latent viruses such as cytomegalovirus are normally held in abeyance by cellular and immune surveillance mechanisms which if impaired, for example by immunosuppressive medications, often result in viral reactivation, replication, and virally-mediated tissue injury –. Sepsis impairs innate and adaptive immunity by multiple mechanisms including apoptosis-induced depletion of immune effector cells and induction of T-cell exhaustion thereby possibly predisposing to viral reactivation and dissemination –. …”
12) NCI and US Army Ft Detrick Pathologist Paul Duray on the CSF cells looking like "Epstein-Barr-like transformed cells" in IDSA's 1989 Reviews Supplement on Spirochetal Diseases:
Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1487-93.
Clinical pathologic correlations of Lyme disease.
"Immature B cells can also be seen in the spinal fluid. These cells can appear quite atypical- not unlike those of transformed or neoplastic lymphocytes." --
Full Text: http://www.actionlyme.org/IDSA_CLINIPATH_DURAY.htm
NEW, by the NIH: "Surviving Sepsis: Detection and Treatment Advances"
By Carolyn Beans for the National Institutes of Health | August 18, 2014 08:43am ET
"Preventing Secondary Infections
"Some people who survive sepsis can develop secondary infections days or even months later. A research team that included Richard Hotchkiss, Jonathan Green and Gregory Storch of Washington University School of Medicine in St. Louis suspected that this is because sepsis might cause lasting damage to the immune system. To test this hypothesis, the scientists compared viral activation in people with sepsis, other critically ill people and healthy individuals. The researchers looked for viruses like Epstein-Barr and herpes simplex that are often dormant in healthy people but can reactivate in those with suppressed immune systems. [Sepsis Has Long-Term Impact for Older Adults, Study Finds]"
13) Duray again in 1992, in Steve Schutzer's review of the 1992 Cold Spring Harbor Conference on Lyme:
"On occasion, these atypical-appearing large lymphocytes have been misinterpreted in biopsy by several laboratories as cells of a malignant lymphoma or leukemia. Bb antigens, then, may stimulate growth of immature lymphocytic suibsets in some target organs, as well as in the cerebrospinal fluid (Szyfelbein and Ross 1988). Usual bacterial infections do not produce such lymphocytic infiltrates in tissue. ****These immunoblastoid cells in Bb infections at times resemble those found in Epstein-Barr virus infections.**** Does Bb reactivate latent virus infections in tissues? Do some tick inocula harbor simultaneous infectious agents (ixodid ticks can harbor Rickettsiae, Babesia microti, and Ehrlichia bacteria, in addition to Bb), producing multi-agent infections in some hosts? Further studies can clarify these issues by mans of tissue-based molecular probe analysis." -
Paul Duray, NCI, NIH, Ft. Detrick, at the 1992 Cold Spring Harbor Crooks' Conference, published in Steve Schutzer's Lyme Disease: Molecular and Immunologic Approaches. - book.
14) Anthony Fauci on how the LYMErix vaccine (Pam3Cys) was apparently (?) used as an HIV vaccine failed in the same way LYMErix failed, causing immunosuppression and greater susceptibility to disease (HIV's gp120 is Pam3Cys in triplicate at least in the vaccine attempt, apparently - DeFoort):
An HIV Vaccine — Challenges and Prospects
"The initial empirical approach of immunizing with VaxGen's AIDSVax, a recombinant form of the outer glycoprotein-120 (gp120) portion of the HIV envelope, which was based on a strategy that was successful with hepatitis B, failed to protect volunteers from infection, apparently because the vaccine did not induce broadly neutralizing antibodies.3"
"Unexpectedly, post hoc analyses of the STEP trial also found a trend toward a greater number of new infections among vaccine recipients than among placebo recipients."
[DEFOORT Pam3Cys Quadrivalent OspA-HIV, see]
Distinction between HIV-1 and HIV-2 infection using novel synthetic lipopeptide conjugates as antigens in enzyme immunoassays.
Böltz T1, Hummel RP, Tröger W, Rübsamen-Waigmann H, Biesert L, Müller-Lantzsch N, Koch P, Bessler W, Jung G.
"A novel immunoassay technique using synthetic lipopeptide (Pam3Cys-Ser) linked to immunodominant peptide domains of HIV-1 and HIV-2 envelope proteins as an antigen adsorbent has been developed. Attachment of peptides to microtiter plates can be considerably improved with this method by employing the hydrophobic properties of lipopeptide. From the sera of 121 HIV-1 infected patients 117 reacted with Pam3Cys-Ser-[HIV-1(598-609)cyclic disulfide]. Five of 5 HIV-2 positive sera were positive with Pam3Cys-Ser-[HIV-2(593-603)cyclic disulfide]. Control sera failed to react with these conjugates.
So, what does that mean? They made an HIV vaccine out of the same structure as the fungal OspA- LYMErix?,... and did not know this would not work because Yale lied to the FDA and the journals about the outcome of LYMErix? How did these patients test positive to the new Pam3Cys antigen while everyone with Lyme does not, especially later in the disease. Were these HIV patients all NEW HIV patients? No way to know at present, since there is no available structure of HIV's gp120 that we can find.
The Koreans found Pam3Cys sticks to itself? >>
That OspA sticks to itself explains why the Western Blots in LYMErix-and ImmuLyme-vaccinated people had unreadable Western Blots with the Blot-Smudging?
PERSING WITH SIGAL EXPLAINING THAT THE WESTERN BLOTS WERE UNREADABLE due to the blot smudging (probably due to OspA sticking to itself, which Alan Barbour reported a long time ago, yet he is the owner of the ImmuLyme OspA vaccine patent), 2000:
Detection of Multiple Reactive Protein Species by Immunoblotting after Recombinant Outer Surface Protein A Lyme Disease Vaccination
A Fauci patent for the
treatment of immune suppression outcomes of bacterial, viral, and fungal
"FIELD OF THE INVENTION
"The present invention pertains to a method for activating the immune
system of a patient by intermittently administering interleukin-2 (IL-2)
to that patient. Such administration of IL-2 can optionally be combined
with other therapies, such as anti-retroviral, anti-bacterial or
anti-fungal therapies, suitable for treatment of the patient's
condition. This invention also relates to an approach to gene therapy
that entails administering IL-2 to a patient so as to facilitate in situ
lymphocyte transduction by a retroviral vector also administered to the
"BACKGROUND OF THE INVENTION
"....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
15) EVERYONE READ THIS, AND THE RELATED ARTICLES ON THE PLOS WEBSITE LINKED ON THE RIGHT in this article; THIS IS LYMERIX-DISEASE (TLR2-agonist, or bacterial lipoprotein and NOT LPS) OR POST-LYME SEPSIS,
MicrRNA-146a Is Upregulated by and Negatively Regulates TLR2 Signalling
"Pre-exposure of monocytes/macrophages (in vitro) or the host (in vivo) to LPS or endotoxin induces a transient state of cellular hyporesponsiveness to a secondary LPS challenge with diminished production of proinflammatory cytokines, thereby conferring protection against LPS-induced lethality and resulting in a significant survival advantage –. This phenomenon is well established and termed endotoxin tolerance. Furthermore, emerging evidence has revealed that modulation of the TLR4-mediated signal transduction pathway is involved in the development of endotoxin tolerance , . For example, down-regulated cell-surface expression of TLR4, reduced interleukin-1 receptor-associated kinase 1 (IRAK-1) expression and myeloid differentiation factor 88 (MyD88)-IRAK immunocomplex formation, and attenuated nuclear factor (NF)-κB activation and mitogen-activated protein kinase (MAPK) phosphorylation are all considered as significant markers for endotoxin tolerance. Therefore, endotoxin tolerance may represent a protective mechanism, whose primary function is to prevent excessive inflammatory response induced by overactivation of the TLR4 signaling pathway. It has been shown that endotoxin tolerance occurs in several disease settings including sepsis, trauma, surgery and pancreatitis ; however, acquisition of endotoxin tolerance may contribute to an increased incidence of secondary bacterial infection in hospitalized patients due to development of an immunesuppressed state , ."
16) Medvedev talking about Immunosuppression from Post-Lyme and Post-LYMErix Sepsis (TLR2-agonists or Pam3Cys is OspA or shed borrelial antigens)
IRAK4 kinase activity is not required for induction of endotoxin tolerance but contributes to TLR2-mediated tolerance
"Development of endotoxin tolerance following the initial “cytokine storm” phase of sepsis is thought to protect the host from an overexuberant immune response and tissue damage but at the same time, may render the host immunocompromised and more susceptible to secondary infection [18,–20]. ...
"Reprogramming  of TLR4 signaling in endotoxin-tolerant monocytes and macrophages does not occur as a result of decreased TLR4 expression but involves altered recruitment, tyrosine phosphorylation, and K63-linked polyubiquitination of proximal receptor-adapter-kinase complexes [22,–27] and induction of negative regulators IRAK-M, SHIP1, and A20 [24, 25, 28]. Although a few studies have sought to dissociate kinase and adapter functions of IRAK4 in IL-1R/TLR signaling, albeit with conflicting results [13,–16, 29,–31], it is unclear how IRAK4 kinase activity affects induction of TLR2 and TLR4 homo- and heterotolerance. To address these questions, we used IRAK4KDKI mice to determine the impact of kinase deficiency of IRAK4 on the induction of TLR tolerance. Our data showed comparable induction of endotoxin tolerance in WT or IRAK4KDKI PMs and BMDMs, as judged by attenuated MAPK phosphorylation, inhibited expression of proinflammatory cytokines and chemokines, and up-regulation of negative TLR regulators, A20 and IRAK-M. Notably, IRAK4 kinase activity was found to be a prerequisite for conferring inhibition of LPS-inducible JNK and p38 MAPK activation following prior exposure to Pam3Cys. These results represent the first systematic analyses of the role of IRAK4 kinase activity in TLR homo- and heterotolerance and pave the way for improved understanding of how IRAK4 kinase dysregulation may underlie immunocompromised states in late sepsis."
17) RE-PROGRAMMING WATSON - with the OspA data, LOL; This is funny. p53 is the apoptosis generator/enzyme/kinase, that is inhibited in the first step of nearly all disease, and the very thing I am screaming about for what 10 years? OspA stops the normal activity of p53/p38, LOL. Then read this and the lead-in into it. Yer gonna laff:
IBM Watson Ushers in a New Era of Data-Driven Discoveries
"In a retrospective, peer reviewed study released this week by Baylor College of Medicine and IBM, scientists demonstrated a possible new path for generating scientific questions that may be helpful in the long term development of new, effective treatments for disease. In a matter of weeks, biologists and data scientists using the Baylor Knowledge Integration Toolkit (KnIT), based on Watson technology, accurately identified proteins that modify p53, an important protein related to many cancers, which can eventually lead to better efficacy of drugs and other treatments. A feat that would have taken researchers years to accomplish without Watson's cognitive capabilities, Watson analyzed 70,000 scientific articles on p53 to predict proteins that turn on or off p53's activity. This automated analysis led the Baylor cancer researchers to identify six potential proteins to target for new research. These results are notable, considering that over the last 30 years, scientists averaged one similar target protein discovery per year.
"On average, a scientist might read between one and five research papers on a good day," said Dr. Olivier Lichtarge, the principal investigator and professor of molecular and human genetics, biochemistry and molecular biology at Baylor College of Medicine. "To put this in perspective with p53, there are over 70,000 papers published on this protein. Even if I'm reading five papers a day, it could take me nearly 38 years to completely understand all of the research already available today on this protein. Watson has demonstrated the potential to accelerate the rate and the quality of breakthrough discoveries."
18) This is a Chinese group trying to figger out how to reverse the well-known phenomenon of OspA-, fungal-antigen- induced immunosuppression or OspA-induced fungal antigen tolerance
A20 is critical for the induction of Pam3CSK4-tolerance in monocytic THP-1 cells.
"A20 functions to terminate Toll-like receptor (TLR)-induced immune response, and play important roles in the induction of lipopolysacchride (LPS)-tolerance. However, the molecular mechanism for Pam3CSK4-tolerance is uncertain. Here we report that TLR1/2 ligand Pam3CSK4 induced tolerance in monocytic THP-1 cells. The pre-treatment of THP-1 cells with Pam3CSK4 down-regulated the induction of pro-inflammatory cytokines induced by Pam3CSK4 re-stimulation. Pam3CSK4 pre-treatment also down-regulated the signaling transduction of JNK, p38 and NF-κB induced by Pam3CSK4 re-stimulation. The activation of TLR1/2 induced a rapid and robust up-regulation of A20, suggesting that A20 may contribute to the induction of Pam3CSK4-tolerance. This hypothesis was proved by the observation that the over-expression of A20 by gene transfer down-regulated Pam3CSK4-induced inflammatory responses, and the down-regulation of A20 by RNA interference inhibited the induction of tolerance. Moreover, LPS induced a significant up-regulation of A20, which contributed to the induction of cross-tolerance between LPS and Pam3CSK4. A20 was also induced by the treatment of THP-1 cells with TNF-α and IL-1β. The pre-treatment with TNF-α and IL-1β partly down-regulated Pam3CSK4-induced activation of MAPKs. Furthermore, pharmacologic inhibition of GSK3 signaling down-regulated Pam3CSK4-induced A20 expression, up-regulated Pam3CSK4-induced inflammatory responses, and partly reversed Pam3CSK4 pre-treatment-induced tolerance, suggesting that GSK3 is involved in TLR1/2-induced tolerance by up-regulation of A20 expression. Taken together, these results indicated that A20 is a critical regulator for TLR1/2-induced pro-inflammatory responses."
19) Ray Dattwyler (SUNY-SB) says in 1988 that exposure to Lyme or even just its supernatants (OspA-like molecules) turn off the NK cell activity (or is immunosuppressive): http://actionlyme.org/TRAINER_2012SUMMER.htm
Modulation of natural killer cell activity by Borrelia burgdorferi. - 1988
Golightly M, Thomas J, Volkman D, Dattwyler R.Department of Pathology, State University of New York, Stony Brook 11794.PMID: 3056196 [PubMed - indexed for MEDLINE]Ann N Y Acad Sci. 1988;539:103-11.
"Effect of B burgdorferi Culture on Normal PBL
"..when lymphocytes are cultured in the presence of growing Bb there is a marked inhibition ( p < .0005 ) of NK activity on days 3, 5, and 7 when compared to lymphocytes cultured in BSKII media in the absence of spirochetes. This effect is not due to a selective depletion or or toxicity to endogenous NK since viability studies and monoclonal antibodies demonstrate no significant changes after culture with the organism.
"The inhibition is directly attributable to the organism or its supernatants (data not shown)."
Gary Wormser's peer-reviewed article about how OspA was immunosuppressive
Gary Wormser's peer reviewed article about how Dearborn "case definition" detected only 15% of the cases in IgG (9 out of 59):
It's pretty obvious why the majority of the participants at the 1994 Dearborn conference (see below) said Steere's testing proposal that said Lyme was only an HLA-linked arthritis, SUCKED!!!
20) Here is Clifford Harding, the discoverer of the mechanisms of both outcomes of OspA Disease or Lyme Disease [immunosuppression and no antbodies, and the other one, where the HLA-molecule together with the antigen is released as an entirely new antigen called an exosome or a vessicle, but is really a complex against which partial auto-/self- antibodies will be made; and in the case of alyme, particularly Allen Steere's version of autoimmunity against Human Leukocyte antigen (I assume)] talking about how if you have been exposed to Borrelial lipid TLR2-liktigens, you will end up with a null or non-response to other TLR agonists, such as viruses:
TLR2 signaling depletes IRAK1 and inhibits induction of type I IFN by TLR7/9.
J Immunol. 2012 Feb 1;188(3):1019-26. doi: 10.4049/jimmunol.1102181. Epub 2012 Jan 6.
Liu YC1, Simmons DP, Li X, Abbott DW, Boom WH, Harding CV.
1Department of Pathology, Case Western Reserve University/University Hospitals Case Medical Center, Cleveland, OH 44106, USA.
"Pathogens may signal through multiple TLRs with synergistic or antagonistic effects on the induction of cytokines, including type I IFN (IFN-I). IFN-I is typically induced by TLR9, but not TLR2. Moreover, we previously reported that TLR2 signaling by Mycobacterium tuberculosis or other TLR2 agonists inhibited TLR9 induction of IFN-I and IFN-I-dependent MHC-I Ag cross processing. The current studies revealed that lipopeptide-induced TLR2 signaling inhibited induction of first-wave IFN-α and IFN-β mRNA by TLR9, whereas induction of second-wave IFN-I mRNA was not inhibited. TLR2 also inhibited induction of IFN-I by TLR7, another MyD88-dependent IFN-I-inducing receptor, but did not inhibit IFN-I induction by TLR3 or TLR4 (both Toll/IL-1R domain-containing adapter-inducing IFN-β dependent, MyD88 independent). The inhibitory effect of TLR2 was not dependent on new protein synthesis or intercellular signaling. IL-1R-associated kinase 1 (IRAK1) was depleted rapidly (within 10 min) by TLR2 agonist, but not until later (e.g., 2 h) by TLR9 agonist. Because IRAK1 is required for TLR7/9-induced IFN-I production, we propose that TLR2 signaling induces rapid depletion of IRAK1, which impairs IFN-I induction by TLR7/9. This novel mechanism, whereby TLR2 inhibits IFN-I induction by TLR7/9, may shape immune responses to microbes that express ligands for both TLR2 and TLR7/TLR9, or responses to bacteria/virus coinfection."
21) Poland 2013 The influence of toll-like receptor stimulation on expression of EBV lytic genes.
Epstein-Barr virus (EBV) establishes latency in the resting memory B-cell compartment. It has been recently suggested that maintenance of chronic infection is dependent on periodic reactivation. Although the stimuli for EBV reactivation in vivo during natural infections are largely unknown, there is evidence indicating that heterologous infections could trigger herpesviruses reactivation. The purpose of this work was to identify the influence of Toll-like receptors stimulation on EBV replication in EBV latently infected Burkitt lymphoma cells (P3HR-1, Raji and Namalwa). The cells were stimulated with Pam3CSK4 (synthetic triacylated lipoprotein), PolyI:C (synthetic analog of dsRNA), LPS (lipopolysaccharide from E.coli), measles virus (MeV) and PMA (phorbol myristate acetate). Non-stimulated cells (NS) served as control. EBV expression was investigated at mRNA level for three viral lytic genes: BZLF1 (immediate early, ZEBRA), BALF2 (early, EA) and BcLF1 (late, VCA). Additionally, the effect of stimulation on NF-kBp65 and inflammatory cytokines (IL-lb, IL-6, IL-8, IL-10, IL-12p70, and TNF) was investigated. Stimulation of TLRs led to limited changes in EBV expression manifesting as increase of ZEBRA at mRNA level in cells treated with PolyI:C and Pam3CSK4. Stimulation with PolyI:C, Pam3CSK4 and LPS also lead to considerable increase of NF-kBp65, while increased levels of inflammatory cytokines were observed for IL-8, TNF and IL-6 in cells treated with PMA and MeV. In conclusion, the results of our experiments support the suggestion that TLRs stimulation with microbial ligands influences EBV virus replication.
Full text pdf : http://www.pjm.microbiology.pl/archive/vol6232013237.pdf <<< Get the full text, seriously, it clarifies much