141119; For People Interested in what the NIH thinks about treatments for Chronic Active Lyme/Epstein-Barr Etc/Chronic Fatigue Syndrome, which are all basically reactivated herpesviruses with fungal antigen-induced immunosuppression...
MEANWHILE, if it is the CDC reporting, you can NOT believe the data. CDC has been caught lying about
1) what Lyme is;
2) changing the definition of Lyme "Disease" to exclude neurologic cases (Dearborn);
3) the CDC continually lies to the public about the Senators’ (Gibson, Blumenthal et al) activity regarding asking the OBM.gov to FORCE the FDA to do their jobs and assure Lyme testing meets their own definition of “valid,” and they lied to the public about the FDA validating Dearborn. The FDA did no such thing. In fact, they objected and said the seronegative patients were the sickest, and said to continue to use the old standard of repeat Western Blots and NO ELISAs (Dattwyler, below);
4) CDC denies the viability of the cyst or spheroplast form of Lyme, while earlier (1964) having been the authors of exactly how to weaponize Borreliae,
5) the CDC was caught throwing out the red and white blood cells to which the mycoplasma or epERTHROzoons as they were formerly called, to which the mycoplasma adhere and invade, when trying to prove Chronic Fatigue Syndrome is not due to mycoplasma (in addition to some combination of herpesviruses);
6) the CDC are lying about the HPV vaccine, giving women a false sense of security against cervical cancer, when the other STDs like chlamydia and mycoplasma cause endometriosis and subsequent infertility. [”Here, take this vaccine and go ahead and be a whore (Secret: Just don’t expect to ever be a mother).”]
7) This is all not to mention all the lies they tell about childhood immunizations (MMR) and how it is the vaccine viruses themselves causing the brain damage we call Autism. SEVEN HUGE LIES like that affecting millions of people worldwide is quite enough to be convinced. You can also assume they know Lyme and LYMErix are the Great Detonators of cancer, MS, ALS, (indirectly thru the other microbes activated by OspA/Borrelia) and everything else because they have been lying about it since Day One, as demonstrated by their deployment of that true moron Allen Steere, originally, to Old Lyme.- KMDickson
1) "Chronic active Epstein-Barr virus infection (CAEBV) is characterised by chronic or recurrent infectious mononucleosis-like symptoms, such as fever, hepatosplenomegaly, persistent hepatitis and extensive lymphadenopathy. Patients with CAEBV have high viral loads in their peripheral blood and/or an unusual pattern of EBV-related antibodies. This disease is rare but severe with high morbidity and mortality. Nearly three decades have passed since this disease was first identified, and recent advances in technology have increased our understanding of CAEBV pathophysiology. There is accumulating evidence that the clonal expansion of EBV-infected T or natural killer (NK) cells plays a central role in the pathogenesis of CAEBV. However, it remains unclear whether CAEBV is truly a monoclonal lymphoproliferative disorder. EBV-infected T or NK cells are able to evade the host cellular immune system due to the limited expression of viral proteins of reduced antigenicity. Recent studies suggest that infection of T or NK cells is a common event during primary EBV infection. A defect or single nucleotide polymorphism in host immune-modulating genes may allow for the expansion of virus infected cells giving rise to CAEBV. In this review, I summarise our current understanding of the pathogenesis of CAEBV and propose a model of CAEBV pathogenicity.
2) RELATED ARTICLES:
3) NIH >> "Optimal Treatment for Chronic Active Epstein-Barr Virus Disease"
"Epstein-Barr virus (EBV) is a ubiquitous virus that infects...
"Most patients with CAEBV present with fever, liver dysfunction, and splenomegaly. About half of patients have lymphadenopathy, thrombocytopenia, and anemia (3). Other frequent symptoms (occurring in 20–40% of patients) include hypersensitivity to mosquito bites, rash, hemophagocytic syndrome, and coronary artery aneurysms. Less common features are calcification of basal ganglia, oral ulcers, lymphoma, interstitial pneumonia, and central nervous system disease. The presence of thromobocytopenia, onset at age 8 or older, and infection of T cells with EBV was associated with a poorer prognosis (5). Death is frequently due to liver failure, malignant lymphoma, or opportunitistic infections.
4) "Characterization and treatment of chronic active Epstein-Barr virus disease: a 28-year experience in the United States."
NIH AGAIN >>
Although patients with CAEBV from Japan have normal or increased numbers of NK cells, many of our patients had reduced NK-cell numbers. Although immunosuppressive agents, rituximab, autologous cytotoxic T cells, or cytotoxic chemotherapy often resulted in short-term remissions, they were not curative. Hematopoietic stem cell transplantation was often curative for CAEBV, even in patients with active lymphoproliferative disease that was unresponsive to chemotherapy. These studies are registered at http://www.clinicaltrials.gov as NCT00032513 for CAEBV, NCT00062868 and NCT00058812 for EBV-specific T-cell studies, and NCT00578539 for the hematopoietic stem cell transplantation protocol.
5) NIH AGAIN >>> "Altered antibody profiles against common infectious agents in chronic disease"
“Despite the important diagnostic value of evaluating antibody responses to individual human pathogens, antibody profiles against multiple infectious agents have not been used to explore health and disease mainly for technical reasons. We hypothesized that the interplay between infection and chronic disease might be revealed by profiling antibodies against multiple agents. Here, the levels of antibodies against a panel of 13 common infectious agents were evaluated with the quantitative Luciferase Immunoprecipitation Systems (LIPS) in patients from three disease cohorts including those with pathogenic anti-interferon-γ autoantibodies (IFN-γ AAB), HIV and Sjögren's syndrome (SjS) to determine if their antibody profiles differed from control subjects. The IFN-γ AAB patients compared to controls demonstrated statistically higher levels of antibodies against VZV (p=0.0003), EBV (p=0.002), CMV (p=0.003), and C. albicans (p=0.03), but lower antibody levels against poliovirus (p=0.04). Comparison of HIV patients with blood donor controls revealed that the patients had higher levels of antibodies against CMV (p=0.0008), HSV-2 (p=0.0008), EBV (p=0.001), and C. albicans (p=0.01), but showed decreased levels of antibodies against coxsackievirus B4 (p=0.0008), poliovirus (p=0.0005), and HHV-6B (p=0.002). Lastly, SjS patients had higher levels of anti-EBV antibodies (p=0.03), but lower antibody levels against several enteroviruses including a newly identified picornavirus, HCoSV-A (p=0.004), coxsackievirus B4 (p=0.04), and poliovirus (p=0.02). For the IFN-γ AAB and HIV cohorts, principal component analysis revealed unique antibody clusters that showed the potential to discriminate patients from controls. The results suggest that antibody profiles against these and likely other common infectious agents may yield insight into the interplay between exposure to infectious agents, dysbiosis, adaptive immunity and disease activity.
PLoS One. 2013 Dec 2;8(12):e81635. doi: 10.1371/journal.pone.0081635. eCollection 2013.
NIH >>> (Same report, full text):
Altered Antibody Profiles against Common Infectious Agents in Chronic Disease
"Moreover, a major gap exists regarding our understanding of whether microbes and viruses, which are not generally recognized to cause chronic illnesses, show more complex interactions in chronic diseases."
“Fungal-Viral Synergy,” anyone?? (referring to the above report) >> "To potentially characterize the interplay between additional infectious agents in these patients compared to controls, we employed LIPS to profile antibodies against 13 different infectious agents including viral and fungal agents." -- yup.
Like LYMErix-like shed Borrelial TLR2/1 agonists activating EBV, ya mean??
Same report, Number 5 above, Authors, participants:
1Clinical Dental Research Core, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland, United States of America
2Western Regional Research Center, U.S. Department of Agriculture, Albany, California, United States of America
3Critical Care Medicine Department, Clinical Center, National Institutes of Health, Bethesda, Maryland, United States of America
4Sjögren Syndrome Clinic, Molecular Physiology and Therapeutics Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland, United States of America
5Department of Perioperative Medicine, Clinical Center, National Institutes of Health, Bethesda, Maryland, United States of America
6Medical Virology Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America
7Center for Infection and Immunity, Columbia University, New York, New York, United States of America
8Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America
Charité-University Medicine Berlin, Germany
6) PubMed Search, all “ EBV DNA and altered immunity “
7) "Detection of viral DNA and immune responses to the human herpesvirus 6 101-kilodalton virion protein in patients with multiple sclerosis and in controls."
"Human herpesvirus 6 (HHV-6), a latent lymphotropic and neurotropic virus, has been suspected as an etiologic agent in multiple sclerosis (MS). The study was undertaken to correlate virologic evidence for HHV-6 activity with the state of host immunity to HHV-6 in MS patients and control subjects. The study revealed that cell-free DNA of HHV-6 was detected more frequently in both serum and cerebrospinal fluid of MS patients than in those of control subjects. T cells recognizing the recombinant 101-kDa protein (101K) corresponding to the major immunoreactive region unique to HHV-6 occurred at significantly lower precursor frequency in MS patients than in control subjects. The resulting HHV-6-specific T-cell lines obtained from MS patients exhibited skewed cytokine profiles characterized by the inability to produce interleukin-4 (IL-4) and IL-10. The decreased T-cell responses to HHV-6 and the altered cytokine profile were consistent with significantly declined serum immunoglobulin G (IgG) titers for HHV-6 of MS patients compared to those of control subjects. In contrast, elevated serum IgM titers for HHV-6 were detected in the majority of MS patients, which may reflect frequent exposure of B cells to HHV-6. The findings suggest that the decreased immune responses to HHV-6 may be responsible for ineffective clearance of HHV-6 in MS patients."
8) 2012 "Association of active human herpesvirus-6, -7 and parvovirus b19 infection with clinical outcomes in patients with myalgic encephalomyelitis/chronic fatigue syndrome."
1August Kirchenstein Institute of Microbiology and Virology, Riga Stradins University, Ratsupites Street 5, LV-1067 Riga, Latvia.
“Frequency of active human herpesvirus-6, -7 (HHV-6, HHV-7) and parvovirus B19 (B19) infection/coinfection and its association with clinical course of ME/CFS was evaluated. 108 ME/CFS patients and 90 practically healthy persons were enrolled in the study. Viral genomic sequences were detected by PCR, virus-specific antibodies and cytokine levels-by ELISA, HHV-6 variants-by restriction analysis. Active viral infection including concurrent infection was found in 64.8% (70/108) of patients and in 13.3% (12/90) of practically healthy persons. Increase in peripheral blood leukocyte DNA HHV-6 load as well as in proinflammatory cytokines' levels was detected in patients during active viral infection.
" Definite relationship was observed between active betaherpesvirus infection and subfebrility, lymphadenopathy and malaise after exertion, and between active B19 infection and multijoint pain. Neuropsychological disturbances were detected in all patients. The manifestation of symptoms was of more frequent occurrence in patients with concurrent infection. The high rate of active HHV-6, HHV-7 and B19 infection/coinfection with the simultaneous increase in plasma proinflammatory cytokines' level as well as the association between active viral infection and distinctive types of clinical symptoms shows necessity of simultaneous study of these viral infections for identification of possible subsets of ME/CFS."
OKay, this keeps coming up, so we can start over at the beginning - the Issue of the 15% vs the 85% and HLA positive (15%, associated with Lyme arthritis or RA) vs HLA-negative (85% NORMAL people who won't make antibodies against most OspA-like antigens shed all the time by spirochetes, which first behaves like flak, and later turns off the immune response in an outcome called tolerance or immunosuppression).
There are 3 different things you have to look at (with your *eyeballs* - there is no way around this, science is 3D) and they are: the USDOJ Lyme RICO complaint, the PacMan Guys, and the real Khan Academy video on "Professional Antigen Presenting Cells."
So, where does HLA vs non-HLA come from? It started back in the day when they were beginning to transplant organs and tissue and found you have to have compatibility between the donor and the recipient - or histo (tissue) compatibility.
So they had to categorize tissue types, and they found, for instance a tendency towards rheumatoid arthritis or allergies were genetic and heritable. And what was that heritable immune thing?
It was determined to be the HLA molecules or the "Human Leukocyte Antigens" (antigen is a bad word for this, because it confuses people with real antigens, which means foreign material; a transplanted tissue with HLAs from an incompatible source, you get it, would be rejected like an antigen).
So, like I tell everyone, go to the real Khan Academy and watch at least the video on "Professional Antigen Presenting Cells." You will find that what the HLA molecules do (clam shaped), is "present" antigen (the real kind, usually), against which the B cells will make antibodies... that is the normal or typical case.
Then look at the 2 PacMan graphics and READ THE TEXT ASSOCIATED with the graphics. The first one shows what the Khan Academy shows. The second one shows what happens if you have Steere's HLAs or Rheumatoid Arthritis HLAs or the HLAs associated with some other "autoimmune" or hypersensitibty (allergy) response-- the 15%. And then I say THIS DOES NOT HAPPEN (antigen is presented - does not happen) in late Lyme in the 85%
Then look at the RICO complaint and see WITH YOUR EYEBALLS the 2 Western Blot outcomes: the 85% or neurological Lyme is on the LEFT, and the Steere's HLA's is on the RIGHT. You will SEE WITH YOUR EYEBALLS a big difference in antibody concentration (the one on the right, arthritis makes a lot of antibodies so the WB bands are darker and there are more of them).
So, what happened was the OspA vaccine was making people sick with a disease like we have - and not so much arthritis, it was a systemic disease outcome, contrary to what is in the popular literature) - in Phase I and Phase II trials, prior to 1994 and Dearborn... Get it?
Dearborn was intended to throw out those systemic adverse events, and they did. Just like us. The expensive kind of Lyme, that is a CNS disease, and we later found out was due to something else - probably EBV reactivated, and EBV is obviously a neurological infection - was thrown out. Kaiser Permanente and The Blues did not want to pay for this, so THEY were the ones screaming for a vaccine, and not us, again, as falsely claimed.
Think about it - the sick people are already sick, so what good is a vaccine going to do them? *We* were not the ones asking for a vaccine, we wanted a cure... Just like today, we have the same trouble: People are less interested in getting this thing STOPPED and the crooks BUSTED, and they say so all the time. They say, "I only want to get better, I am not interested in all the bullshit," not thinking of course, that *WE* would like to get better too, duh.
So, now, look at the following for items you need to review.
Khan Academy on Professional Antigen Presenting Cells (does not happen after a while if the antigen is fungal like OspA oe like shed Borrelial antigen or TLR2/1 agonists:
Compare to the 2 Pac Man guys, graphics.
http://www.actionlyme.org/USDOJ_COMPLAINT_RICO.htm << See the Western Blots – but it’s 15% not 30% who have the Steere/Rheumatoid Arthritis HLAs.
^^^ That is related. It shows the CDC is lying about Dearborn being FDA approved. The FDA never approved this, in fact, they never looked to see if Dearborn was validated. I know because I asked them, and their answer was that they are not FORCED to assure the testing used was validated, Now they are being FORCED to as re Lyme, per Senator Blumenthal et al. Follow? ILADS and the LDA are totally clueless and are giving out the WRONG information.
The 85% are normal people who do not have Steere's rheumatoid arthritis predisposition or HLAs. So, they're "negative to Steere's arthritis HLAs."
Steere and the CDC say you are not allowed to have "Lyme Disease" unless you have the rheumatoid arthritis-associated HLAs or the high antibody response.
The CDC and their associated ALDF.com/IDSA/Yale/NYMC Lyme crooks also say those people only have arthritis in one or two joints, but no fatigue or neurological signs (Klempner and Wormser, as shown below)). It was said at the 1998 FDA meeting by Vijay Sikand that the people with Lyme arthritis make enough antibodies to fight off the disease (and are not as sick).
The Lyme crooks don’t care if NYMC gets sued because that’s a Catholic Hospital and most of the Lyme crooks are Israelis.