Blowing the Whistle at the FDA, Jan 2001, exposing Dearborn and how OspA causes immunosuppression rather than, "was a vaccine."

01 Oct 2017


File List, RICO

1988 Steere says Lyme is like a B cell leukemia

Assoc Blogs-n-Webs:




Fungal Exosomes Inhibit Apoptosis

IDSA: "Vaccines serve the mfgs, not their victims"


BlumenthalAntiTrust Lawsuit

Exosomes, Blebs


CDC Admits Fraud, 2016
Dattwyler, 1988
Golightly, 1988
Dressler, 1994
BarbourFish, 1993
Dearborn, 1994

Pathogenic Fungi

Bush's warcrimes, Oct 2000




Chronic Pain and Disease without Classical HLA-linked Autoimmune "inflammation" (see the Pac Man guys)

By Kathleen Dickson on Sunday, November 23, 2014 at 5:44am

Our goal here is to counter the claim by the CDC, the Lyme crooks, and the American Psychiatric Association who falsely claim that you can't have a "disease" unless you have the classical HLA-linked hypersensitivity response and their version of "autoimmunity" with the too-many-antbodies and a heritable, genetic, Major Histocompatability (MHC or HLA) link.

Again, you are not allowed to have a "disease" unless it is HLA-associated with too many antibodies. Everything else, like Lyme, CFIDS, etc, is labeled psychiatric, or the newer terminology "neuro-immune," but "neuro-immune" is code language for "psychiatric." Currently all the focus on further abusing people with severe, multiple infections (Lyme, Fibro, CFIDS) is to say there is a gene link to "crazy-in-the-brain."

This file will be incorporated into the one working @ Khan Academy of Lyme, section 4.

The reason for this fraud - the abuse of CFIDS, Fibromyalgia, Lyme, ME, Gulf War Illness Victims, and the Medical Kidnapees like Justina Pelletier - has to do with covering up the mechanisms of the Autism-From-Vaccines-Pandemic (also fungal-viral synergy, and now also called "post-sepsis syndrome" but this post-sepsis syndrome is by definition, a state of chronic active herpes and other infections. And that data can be found here:

Mol Neurobiol. 2012 Dec;46(3):614-38. doi: 10.1007/s12035-012-8320-7. Epub 2012 Aug 17.
Infectious agents and neurodegeneration.

"A growing body of epidemiologic and experimental data point to chronic bacterial and viral infections as possible risk factors for neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis. Infections of the central nervous system, especially those characterized by a chronic progressive course, may produce multiple damage in infected and neighbouring cells. The activation of inflammatory processes and host immune responses cause chronic damage resulting in alterations of neuronal function and viability, but different pathogens can also directly trigger neurotoxic pathways. Indeed, viral and microbial agents have been reported to produce molecular hallmarks of neurodegeneration, such as the production and deposit of misfolded protein aggregates, oxidative stress, deficient autophagic processes, synaptopathies and neuronal death. These effects may act in synergy with other recognized risk factors, such as aging, concomitant metabolic diseases and the host's specific genetic signature. This review will focus on the contribution given to neurodegeneration by herpes simplex type-1, human immunodeficiency and influenza viruses, and by Chlamydia pneumoniae."


J Virol. 1999 Oct;73(10):8817-23.
Localization of a passively transferred human recombinant monoclonal antibody to herpes simplex virus glycoprotein D to infected nerve fibers and sensory neurons in vivo.

"A human recombinant monoclonal antibody to herpes simplex virus (HSV) glycoprotein D labeled with the fluorescent dye Cy5 was administered to mice infected in the cornea with HSV type 1 (HSV-1). The distribution of such antibody in the corneas and trigeminal ganglia of the mice was then investigated by confocal microscopy. The antibody was detected on HSV-infected nerve fibers in the cornea--identified by colocalization with HSV antigens and the neuritic markers neurofilament, GAP-43, synapsin-1, and CNPase--and on the perikarya of sensory neurons in the HSV-1-infected neurons in ipsilateral trigeminal ganglia. Antibodies have been shown to be effective against many neurotropic viruses, often in the absence of obvious cell damage. Observations from experimental HSV infections suggest that antibodies could act in part by interfering with virus expression in the ganglia and/or with axonal spread. The present results provide morphological evidence of the localization of antiviral antibodies at anatomical sites relevant to such putative antibody-mediated protective actions and suggest that viral glycoproteins are accessible to antibodies on infected nerve fibers and sensory neurons."

Right now I am working from this and finding the other herpes, like zoster and simplex more often associated with chronic nerve pain; not sure what that means... whether this is about lack of investigation or we are sporting more than just CMV, EBV, and HHV-6, which most Lyme victims have said they have elevated antibodies to (perhaps not the cut-off for acute stage, but still):


New from the NIH: Talks about treatment for chronic active herpes viruses as the cause of Multiple Sclerosis:

PLoS One. 2014 Aug 22;9(8):e105434. doi: 10.1371/journal.pone.0105434. eCollection 2014.
A complex role of herpes viruses in the disease process of multiple sclerosis.
Wuest SC1, Mexhitaj I1, Chai NR1, Romm E1, Scheffel J2, Xu B3, Lane K3, Wu T4, Bielekova B1.
Author information
1Neuroimmunological Diseases Unit, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America.
2Molecular Immunology Section, Laboratory of Molecular Immunogenetics, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
3Imaging Probe Development Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
4Clinical Neurosciences Program, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America.

"Multiple sclerosis (MS) is a chronic inflammatory disorder of the central nervous system (CNS). Neither the antigenic target(s) nor the cell population(s) responsible for CNS tissue destruction in MS have been fully defined. The objective of this study was to simultaneously determine the antigen (Ag)-specificity and phenotype of un-manipulated intrathecal CD4+ and CD8+ T cells of patients with relapsing-remitting and progressive MS compared to subjects with other inflammatory neurological diseases. We applied a novel Ag-recognition assay based on co-cultures of freshly obtained cerebrospinal fluid T cells and autologous dendritic cells pre-loaded with complex candidate Ag's. We observed comparably low T cell responses to complex auto-Ag's including human myelin, brain homogenate, and cell lysates of apoptotically modified oligodendroglial and neuronal cells in all cohorts and both compartments. Conversely, we detected a strong intrathecal enrichment of Epstein-Barr virus- and human herpes virus 6-specific (but not cytomegalovirus-specific) reactivities of the Th1-phenotype throughout all patients. Qualitatively, the intrathecal enrichment of herpes virus reactivities was more pronounced in MS patients. This enrichment was completely reversed by long-term treatment with the IL-2 modulating antibody daclizumab, which strongly inhibits MS disease activity. Finally, we observed a striking discrepancy between diminished intrathecal T cell proliferation and enhanced cytokine production of herpes virus-specific T cells among progressive MS patients, consistent with the phenotype of terminally differentiated cells. The data suggest that intrathecal administration of novel therapeutic agents targeting immune cells outside of the proliferation cycle may be necessary to effectively eliminate intrathecal inflammation in progressive MS."



J Virol. 2014 Nov 1;88(21):12740-51. doi: 10.1128/JVI.02106-14. Epub 2014 Aug 20.
Gammaherpesvirus Latency Differentially Impacts the Generation of Primary versus Secondary Memory CD8+ T Cells during Subsequent Infection.


"CD8(+) T cells are critical for the clearance of intracellular pathogens, including viruses, certain bacteria, and tumors. However, current models for memory CD8(+) T cell differentiation are derived from pathogen-free laboratory mice challenged with a single pathogen or vaccine vector. Unlike laboratory animals, all humans are infected with multiple acute and chronic pathogens, including the highly prevalent herpesviruses Epstein-Barr virus (EBV), cytomegalovirus (CMV), herpes simplex viruses (HSV), and varicella-zoster virus (VZV). The purpose of these studies was to determine the effect of gammaherpesvirus latency on T cell number and differentiation during subsequent heterologous viral infections. We observed that ongoing gammaherpesvirus latency affects the number and phenotype of primary versus secondary memory CD8(+) T cells during acute infection. These results suggest that unlike pathogen-free laboratory mice, infection or immunization of latently infected humans may result in the generation of T cells with limited potential for long-term protection."

^^^ As you can see, the disease paradigm is shifting to the more rational - stuff we learned from the OspA vaccines outcomes :) Also TOO MANY VACCINES, anyone?

More science on Vit C for chronic EBV:

Oh, look yet another genius paradigm-shifter (the original connection to Burkitt's Lymphoma was between EBV and Malaria - immune suppressor with TLR2-agonists, but he shifts it over to HIV to make it independent brilliance):

Semin Cancer Biol. 2014 Jun;26:99-115. doi: 10.1016/j.semcancer.2014.04.004. Epub 2014 Apr 18.
Co-infections, inflammation and oncogenesis: future directions for EBV research.
Rickinson AB.
School of Cancer Sciences, University of Birmingham, Birmingham, UK. Electronic address:

"Epstein-Barr virus (EBV) is aetiologically linked to a wide range of human tumours. Some arise as accidents of the virus' lifestyle in its natural niche, the B lymphoid system; these include B-lymphoproliferative disease of the immunocompromised, Hodgkin Lymphoma, Burkitt Lymphoma and particular forms of diffuse large B cell lymphoma. Interestingly, HIV infection increases the incidence of each of these B cell malignancies, though by different degrees and for different reasons. Other EBV-associated tumours arise through rare viral entry into unnatural target tissues; these include all cases of nasal T/NK cell lymphoma and of undifferentiated nasopharyngeal carcinoma plus a small but significant subset of gastric carcinomas, a tumour type more generally associated with chronic Helicobacter pylori infection. Understanding EBV's involvement in the pathogenesis of these different malignancies is an important long-term goal. This article focuses on two overlapping, but relatively neglected, areas of research that could contribute to that goal. The first addresses the mechanisms whereby coincident infections with other pathogens increase the risk of EBV-positive malignancies, and takes as its paradigm the actions of holoendemic malaria and HIV infections as co-factors in Burkitt lymphomagenesis. The second widens the argument to include both infectious and non-infectious sources of chronic inflammation in the pathogenesis of EBV-positive tumours such as T/NK cell lymphoma, nasopharyngeal carcinoma and gastric carcinoma."


Indian J Hematol Blood Transfus. 2014 Mar;30(1):26-8. doi: 10.1007/s12288-012-0207-2. Epub 2012 Oct 25.
Epstein-barr virus infection masquerading as acute leukemia: a report of two cases and review of literature.
Chhabra P1, Law AD1, Sharma U2, Suri V1, Sachdeva MS3, Kumari S1, Varma S1, Malhotra P1.

"Epstein-Barr virus (EBV) is the first herpes virus to be completely sequenced. It is implicated in diseases from the benign infectious mononucleosis to malignant nasopharyngeal carcinoma, Burkitt's lymphoma and primary CNS lymphoma in AIDS patients. It has also been found to be associated with some miscellaneous diseases like chronic fatigue syndrome, multiple sclerosis etc. however causality still remains an issue of debate. As the virus mainly targets the lymphomonuclear cells and the reticuloendothelial system of the body, it's various manifestations are often mistaken as leukemic malignancies. We report two such cases of young adults who had been diagnosed as having acute leukemia on the basis of atypical cells in the peripheral blood. One patient later turned out to be a classical infectious mononucleosis and second patient had EBV associated hemophagocytic lymphohistiocytosis syndrome."

Chronic Lyme ^^^ is identical to CLL in symptoms with the extrme fatigue, so you have to look out for that proliferation - CLD being really about Chronic Active EBV/Similar Herpesviruses.


This we already saw and was on my website, reverse correlation with EBV antibodies and chronic fatigue syndrome, which fits our paradigm, as we have said before:

PLoS One. 2014 Jan 15;9(1):e85387. doi: 10.1371/journal.pone.0085387. eCollection 2014.
Deficient EBV-specific B- and T-cell response in patients with chronic fatigue syndrome.
Loebel M1, Strohschein K2, Giannini C1, Koelsch U3, Bauer S1, Doebis C4, Thomas S1, Unterwalder N3, von Baehr V4, Reinke P5, Knops M1, Hanitsch LG1, Meisel C6, Volk HD7, Scheibenbogen C7.
1Institute for Medical Immunology, Charité University Medicine Berlin, Campus Virchow, Berlin, Germany.
2Institute for Medical Immunology, Charité University Medicine Berlin, Campus Virchow, Berlin, Germany ; Julius Wolff Institute, Charité University Medicine Berlin, Campus Virchow, Berlin, Germany.
3Labor Berlin GmbH, Immunology Department, Charité University Medicine Berlin, Campus Virchow, Berlin, Germany.
4Institute for Medical Diagnostics, Berlin, Germany.
5Berlin-Brandenburg Center for Regenerative Therapies (BCRT), Charité University Medicine Berlin, Germany ; Department Nephrology, Charité University Medicine Berlin, Germany.
6Institute for Medical Immunology, Charité University Medicine Berlin, Campus Virchow, Berlin, Germany ; Labor Berlin GmbH, Immunology Department, Charité University Medicine Berlin, Campus Virchow, Berlin, Germany.
7Institute for Medical Immunology, Charité University Medicine Berlin, Campus Virchow, Berlin, Germany ; Berlin-Brandenburg Center for Regenerative Therapies (BCRT), Charité University Medicine Berlin, Germany.

"Epstein-Barr virus (EBV) has long been discussed as a possible cause or trigger of Chronic Fatigue Syndrome (CFS). In a subset of patients the disease starts with infectious mononucleosis and both enhanced and diminished EBV-specific antibody titers have been reported. In this study, we comprehensively analyzed the EBV-specific memory B- and T-cell response in patients with CFS. While we observed no difference in viral capsid antigen (VCA)-IgG antibodies, EBV nuclear antigen (EBNA)-IgG titers were low or absent in 10% of CFS patients. Remarkably, when analyzing the EBV-specific memory B-cell reservoir in vitro a diminished or absent number of EBNA-1- and VCA-antibody secreting cells was found in up to 76% of patients. Moreover, the ex vivo EBV-induced secretion of TNF-α and IFN-γ was significantly lower in patients. Multicolor flow cytometry revealed that the frequencies of EBNA-1-specific triple TNF-α/IFN-γ/IL-2 producing CD4(+) and CD8(+) T-cell subsets were significantly diminished whereas no difference could be detected for HCMV-specific T-cell responses. When comparing EBV load in blood immune cells, we found more frequently EBER-DNA but not BZLF-1 RNA in CFS patients compared to healthy controls suggesting more frequent latent replication. Taken together, our findings give evidence for a deficient EBV-specific B- and T-cell memory response in CFS patients and suggest an impaired ability to control early steps of EBV reactivation. In addition the diminished EBV response might be suitable to develop diagnostic marker in CFS."


Here they talk about Lyme as if it is advance aging - which we have said before and they also talk about badly cloned B cells - something we also talk about all the time but say it does not go as far in most cases as leukemia (so they say the same things we say, verifying independently our observations):

J Immunol. 2014 Jan 15;192(2):603-11. doi: 10.4049/jimmunol.1301384. Epub 2013 Dec 11.
Effects of aging, cytomegalovirus infection, and EBV infection on human B cell repertoires.
Wang C1, Liu Y, Xu LT, Jackson KJ, Roskin KM, Pham TD, Laserson J, Marshall EL, Seo K, Lee JY, Furman D, Koller D, Dekker CL, Davis MM, Fire AZ, Boyd SD.
1Department of Pathology, Stanford University, Stanford, CA 94305;

"Elderly humans show decreased humoral immunity to pathogens and vaccines, yet the effects of aging on B cells are not fully known. Chronic viral infection by CMV is implicated as a driver of clonal T cell proliferations in some aging humans, but whether CMV or EBV infection contributes to alterations in the B cell repertoire with age is unclear. We have used high-throughput DNA sequencing of IGH gene rearrangements to study the BCR repertoires over two successive years in 27 individuals ranging in age from 20 to 89 y. Some features of the B cell repertoire remain stable with age, but elderly subjects show increased numbers of B cells with long CDR3 regions, a trend toward accumulation of more highly mutated IgM and IgG Ig genes, and persistent clonal B cell populations in the blood. Seropositivity for CMV or EBV infection alters B cell repertoires, regardless of the individual's age: EBV infection correlates with the presence of persistent clonal B cell expansions, whereas CMV infection correlates with the proportion of highly mutated Ab genes. These findings isolate effects of aging from those of chronic viral infection on B cell repertoires and provide a baseline for understanding human B cell responses to vaccination or infectious stimuli."

Harvard agrees with our model (It's not an autoimmune disease but chronic active EBV and a B cell disease):

Epstein–Barr virus in the development of multiple sclerosis
March 2008, Vol. 8, No. 3 , Pages 331-333 (doi:10.1586/14737175.8.3.331)

Alberto AscherioHarvard School of Public Health, Departments of Nutrition and Epidemiology, 655 Huntington Avenue, Boston, MA 02115, USA. aascheri@hsph.harvard.eduRead More:


High % of responders to antiviral drugs in Chronic Fatigue Syndrome:

J Med Virol. 2013 Dec;85(12):2101-9. doi: 10.1002/jmv.23713. Epub 2013 Aug 19.
Randomized clinical trial to evaluate the efficacy and safety of valganciclovir in a subset of patients with chronic fatigue syndrome.
Montoya JG1, Kogelnik AM, Bhangoo M, Lunn MR, Flamand L, Merrihew LE, Watt T, Kubo JT, Paik J, Desai M.
Author information
1Department of Medicine, Stanford University School of Medicine, Stanford, California; Division of Infectious Diseases and Geographic Medicine, Stanford University School of Medicine, Stanford, California.


"There is no known treatment for chronic fatigue syndrome (CFS). Little is known about its pathogenesis. Human herpesvirus 6 (HHV-6) and Epstein-Barr virus (EBV) have been proposed as infectious triggers. Thirty CFS patients with elevated IgG antibody titers against HHV-6 and EBV were randomized 2:1 to receive valganciclovir (VGCV) or placebo for 6 months in a double-blind, placebo-controlled trial. Clinical endpoints aimed at measuring physical and mental fatigue included the Multidimensional Fatigue Inventory (MFI-20) and Fatigue Severity Scale (FSS) scores, self-reported cognitive function, and physician-determined responder status. Biological endpoints included monocyte and neutrophil counts and cytokine levels. VGCV patients experienced a greater improvement by MFI-20 at 9 months from baseline compared to placebo patients but this difference was not statistically significant. However, statistically significant differences in trajectories between groups were observed in MFI-20 mental fatigue subscore (P = 0.039), FSS score (P = 0.006), and cognitive function (P = 0.025). VGCV patients experienced these improvements within the first 3 months and maintained that benefit over the remaining 9 months. Patients in the VGCV arm were 7.4 times more likely to be classified as responders (P = 0.029). In the VGCV arm, monocyte counts decreased (P




BMJ Case Rep. 2013 Apr 22;2013. pii: bcr2013009171. doi: 10.1136/bcr-2013-009171.
Epstein-Barr virus-associated cerebellar ataxia.
Ali K1, Lawthom C.

"Cerebellar ataxia is a common neurological presentation. It can be acute, subacute or chronic. Neurological complications of Epstein-Barr virus (EBV) are well-recognised with a variety of presentations. Acute cerebellar ataxia is a rare, but an established complication. It has been described as the sole manifestation of EBV infection without the systemic features of infectious mononucleosis. The pathophysiology is not clear. The course of the illness may last for a few months with a benign outcome, though serious complications can happen. We present a case of a 38-year-old man who presented with an acute cerebellar ataxia owing to EBV infection, along with a review of the literature."