Does Israel have open season to eavesdrop on American Government, a contract that might be complete with bribes to politicians, may allow Israel to eavesdrop on all Blackberry, cell phone, and other communications. American daily life could be vastly influenced by secret power out of Israel.
Give credit where credit is due. Israel is probably the best at spying worldwide, in using false flag operations to further their agenda while not looking like they’re not involved, and can covertly silence and discredit those that dare make a peep.
Who is really in control of the US Government? It certainly isn’t the American people, nor is it elected officials, as the American Investigators/Law Enforcement and the US Kangaroo skewed and out of control courts have rendered most elected officials impotent.
Elected officials are just for show, there is no Freedom or protection of American Rights of Americans in America, and those who suffer at American hands worldwide know that America is no protector of human rights, but is growing in stature as a bigger and bigger bully, violating Human and Civil Rights, all while squashing Free Speech and Free Expression. The media is merely a propaganda machine.
It is possible that Israel has dirt on every single Federal Elected Official and maybe other officials such as those in the Pentagon, are under Israeli surveillance, and speaking out about Israel, the amount of US taxpayer dollars that goes to Israel, and being critical of any of Israel’s policies or behavior could be very detrimental to one’s life, reputation, and ability to work. Even being slightly critical of Israel, in a debate, can label one for life as Anti-Semitic.
The world sees our equipment, American Dollars, and our blind support for anything that Israel does or says through its leaders. All over the world, America is known as Israel’s puppet.
Do you remember a Mad Max sequel that had a character call, “Master-Blaster,” where a midget rode atop a very physically strong fighter in Roman Style gladiator games, to be exposed as being mentally challenged. “Blaster” was exposed when his mask came off, and “Master” then had no power.
Betty Dodson 03 Aug 06
National Health Fraud Coordinator ActionLyme.org
Food and Drug Administration
5600 Fishers Lane, Room 12-07
Rockville, MD 20857
FAX: (301) 443-2143
The Testing for “Lyme Disease” Remains Deliberately Fraudulent
The nature of this complaint is about the testing for Lyme disease, which remains fraudulent, but was fraudulently created to falsely qualify the Lyme vaccines. OspA and B were left out of the diagnostic standard (RICO) and B31 expresses little or no OspC (fraud).
The persons centrally involved in changing the definition of Lyme disease from that of a local Northeast borreliosis to a temporary arthritis in a knee are Allen Steere, Edward McSweegan, Yale and UCONN staff, and Alan Barbour.
From my website you can see who was on the panel to approve the bogus testing for Lyme disease at the October 1994 Dearborn CDC meeting on the diagnostic standard:
http://www.actionlyme.org/Dearborn_Who_Approved.htm (all links are case-sensitive)
This Oct 1994 CDC meeting took place after the Jun 1994 FDA meeting on the testing for Lyme disease, in which Ray Dattwyler suggested that the testing for Lyme disease after 1994 be the same as it was before 1994, and that is, to perform serial Western Blots to look for changing and expanding IgM and IgG antibodies. This criteria was the CDC’s original (1990) standard (because this is a relapsing fever borreliosis- and the meaning of the relapse is the production of new antigens and therefore antibodies), and to keep that testing schema of performing serial Western Blots was Dattwyler’s recommendation to the FDA as you can see:
1) http://www.actionlyme.org/CDC_DOCUMENTS_1990.htm Old CDC standard
2) http://www.actionlyme.org/Dattwyler_Luft_Bb_DNA_in_CSF.htm = Dattwyler and Luft say to the 1994 FDA committee,
“A rising serologic response would suggest and infection. I think it would be true about serial Western Blots where one would see an increase repertoire of immune response against various antigens to the borrelia.”
Allen Steere had originally proposed that the testing for Lyme disease be…
“Using immunoblots, we identified proteins of Borrelia burgdorferi bound by IgM and IgG antibodies during Lyme disease. In 12 patients with early disease alone, both the IgM and IgG responses were restricted primarily to a 41-kD antigen. This limited response disappeared within several months. In contrast, among six patients with prolonged illness, the IgM response to the 41-kD protein sometimes persisted for months to years, and late in the illness during arthritis, a new IgM response sometimes developed to a 34-kD component of the organism. The IgG response in these patients appeared in a characteristic sequential pattern over months to years to as many as 11 spirochetal antigens. The appearance of a new IgM response and the expansion of the IgG response late in the illness, and the lack of such responses in patients with early disease alone, suggest that B. burgdorferi remains alive throughout the illness.” --
Antigens of Borrelia burgdorferi recognized during Lyme disease. Appearance of a new immunoglobulin M response and expansion of the immunoglobulin G response late in the illness. J Clin Invest. 1986 Oct;78(4):934-9
…serial Western Blots.
We now know that the only validated method to detect Lyme borreliosis- or ANY borreliosis- is through the detection of genera-specific antibodies to flagellin.
Yale validated the following flagellin 1991 method according to FDA rules, and this is the 1) earliest, 2) most accurate (17/18 = 94.4% accurate) and was made 3) specific, per FDA rules for the validation of an analytical method.
It was patented under US patents 5, 616, 533:
Infect Immun. 1991 Oct;59(10):3531-5
Molecular characterization of the humoral response to the 41-kilodalton flagellar antigen of Borrelia burgdorferi, the Lyme disease agent.
Berland R, Fikrig E, Rahn D, Hardin J, Flavell RA.
Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06510.
The earliest humoral response in patients infected with Borrelia burgdorferi, the agent of Lyme disease, is directed against the spirochete's 41-kDa flagellar antigen. In order to map the epitopes recognized on this antigen, 11 overlapping fragments spanning the flagellin gene were cloned by polymerase chain reaction and inserted into an Escherichia coli expression vector which directed their expression as fusion proteins containing glutathione S-transferase at the N terminus and a flagellin fragment at the C terminus. Affinity-purified fusion proteins were assayed for reactivity on Western blots (immunoblots) with sera from patients with late-stage Lyme disease. The same immunodominant domain was bound by sera from 17 of 18 patients. This domain (comprising amino acids 197 to 241) does not share significant homology with other bacterial flagellins and therefore may be useful in serological testing for Lyme disease.
PMID: 1894359 [PubMed - indexed for MEDLINE]
The claim of the patent is the validation of the method.
Similarly, Alan Barbour patented a method to diagnose the one of Borreliae in the Lone Star ticks via its specific flagellin.
All of that means band 41 (flagellin) on a Western Blot can be made specific enough to diagnose Lyme or any other borreliosis.
This fact Yale obviously knew in 1991, when they developed their Borrelia burgdorferi specific flagellin method. Yale did not use this Bb-specific-41 method to diagnose Lyme disease in LYMErix vaccinated people and that is because they knew LYMErix did not prevent Lyme disease. For Relapsing Fever organisms, you can never have a vaccine, because the minute you create an antibody against a surface antigen, the bugs create a new class of organisms lacking the antigen for which an antibody has been made. This is also known as “selecting” strains, as Alan Barbour (CDC Epidemiological Intelligence-EIS officer) described here in 1992:
1: J Exp Med. 1992 Sep 1;176(3):799-809.Links
Antibody-resistant mutants of Borrelia burgdorferi: in vitro selection and characterization.
· Sadziene A, Rosa PA, Thompson PA, Hogan DM, Barbour AG.
Department of Microbiology, University of Texas Health Science Center, San Antonio 78284.
We used polyclonal antisera and monoclonal antibodies (mAbs) to inhibit the growth of clonal populations of two strains of Borrelia burgdorferi, the Lyme disease agent, and thereby select for antibody-resistant mutants. mAbs were directed at the outer membrane proteins, OspA or OspB. Mutants resistant to the growth-inhibiting properties of the antibodies were present in the populations at frequencies ranging from 10(-5) to 10(-2). The several escape variants that were examined were of four classes. Class I mutants were resistant to all mAbs; they lacked OspA and OspB and the linear plasmid that encodes them. Two other proteins were expressed in larger amounts in class I mutants; mAbs to these proteins inhibited the mutant but not the wild-type cells. Class II mutants were resistant to some but not all mAbs; they had truncated OspA and/or OspB proteins. Class III mutants were resistant only to the selecting mAb; they had full-length Osp proteins that were not bound by the selecting antibody in Western blots. In two class III mutants resistant to different anti-OspA mAbs, missense mutations were demonstrated in the ospA genes. Class IV mutants were likewise resistant only to selecting antibody, but in this case the selecting antibody still bound in Western blots.
PMID: 1339462 [PubMed - indexed for MEDLINE]
On my website, I give more links to the data which proves this fraud:
Three times, Yale demonstrated that they could not even tell if their vaccine, LYMErix, worked, and that they could not read their Western Blots in LYMErix-vaccinated people.
They could not tell whether or not LYMErix prevented Lyme earlier than 1996, so they simply lied to the FDA.
1) The 1996 Persing patent
DETAILED DESCRIPTION OF THE INVENTION
"Lyme disease vaccines can be prepared utilizing outer surface protein A (OspA) from B. burgdorferi (E. Fikrig et al., Science, 250:553-6 (1990)). Physiological fluids from a vaccinated subject, such as a human or a domestic animal, can therefore be expected to contain antibodies to OspA. The presence of anti-OspA antibodies in subject serum makes it difficult to detect or confirm an infection by the spirochete B. burgdorferi in vaccinated individuals, because current diagnostic methods are based on a reaction between antibodies in subject serum and an antigen preparation made from a B. burgdorferi cell lysate that contains OspA, which can result in serologic false positive responses.
The present invention provides an antigenic B. burgdorferi preparation lacking a detectable level of OspA. False positive reactions in OspA-vaccinated subjects are eliminated when this antigen preparation is utilized to detect B. burgdorferi infection in such individuals, since the preparation does not react with the anti-OspA antibodies present in the sera due to vaccination."
“The present invention provides a method useful to detect a B. burgdorferi infection in a subject. The method provided by the invention is particularly useful to discriminate B. burgdorferi infection from OspA vaccination, although it is sufficiently sensitive and specific to use in any general Lyme disease screening or diagnostic application. Thus, the method of the invention is particularly appropriate for large scale screening or diagnostic applications where only part of the subject population has been vaccinated or where the vaccination status of the population is unknown. --- This being the “racket.” In 1996 these people clearly knew there would be a problem differentiating people who had Lyme from people who had LYMErix vaccination.
Only Imugen and L2 Diagnostics (Yale’s former Lyme and Lupus Clinic) were to be licensed to use this Persing “No-OspA-B” Method. OspA and B were left out of the Steere/Dressler CDC Dearborn Method which is the current method to diagnose Lyme. Never should they have been left out, and that is just common sense.
OspA is the vaccine because it is 100% specific for Lyme, but you can’t have a diagnosis of Lyme if you have that 100% specific antibody? This is utterly ridiculous. Steere and Yale chose OspA to be the vaccine because they believed “Lyme disease” was a condition of a hypersensitivity reaction to OspA in a knee. This they knew in 1992. Normally we don’t think of giving people a vaccine without warning that 30% of the population will be allergic to it.
1: Infect Immun. 1993 Jul;61(7):2774-9.
Association of treatment-resistant chronic Lyme arthritis with HLA-DR4 and antibody reactivity to OspA and OspB of Borrelia burgdorferi.
· Kalish RA,Leong JM, Steere AC.
Division of Rheumatology/Immunology, New England Medical Center, Tufts University School of Medicine, Boston, Massachusetts 02111.
Chronic Lyme arthritis that is unresponsive to antibiotic therapy is associated with an increased frequency of the HLA-DR4 specificity. To determine whether the immune response to a particular polypeptide of Borrelia burgdorferi may be associated with treatment-resistant chronic Lyme arthritis, we correlated the clinical courses and HLA-DR specificities of 128 patients with Lyme disease with their antibody responses to spirochetal polypeptides. Antibody reactivity was determined by Western blotting (immunoblotting) with sonicated whole B. burgdorferi and recombinant forms of its outer surface proteins, OspA and OspB, as the antigen preparations. Of 15 patients monitored for 4 to 12 years, 11 (73%) developed strong immunoglobulin G responses to both OspA and OspB near the beginning of prolonged episodes of arthritis, from 5 months to 7 years after disease onset. When single serum samples from 80 patients with Lyme arthritis, were tested, 57 (71%) showed antibody reactivity to recombinant Osp proteins; in contrast, none of 43 patients who had erythema migrans or Lyme meningitis (P < p =" 0.03)" p =" 0.009);">
PMID: 7685738 [PubMed - indexed for MEDLINE]
2) The 1999/2000 publication where they admit the could not read their Western Blots in LYMErix or OspA vaccinated people because of the Blot-smudging, as this same author, Dave Persing, explains:
“In the case of the FDA-approved immunoblot test kit, the identification of discrete bands at molecular weights >30 kDa is often unreliable or impossible because of the homogeneous staining in this area, compromising the ability of this test to diagnose Lyme disease in vaccinated study subjects. The manufacturer of the only currently FDA-approved (and released) recombinant OspA Lyme disease vaccine [Yale’s LYMErix vaccine-added by KMD] has suggested that vaccination does not interfere with serological evaluation of Lyme disease in vaccine recipientsa statement that is not supported by the data presented here.”
I hope that phrase stands out, since these guys later said:
"It was possible to tell whether or not they had been vaccinated," says David Persing, vice president of research for Corixa, who did the study with Molloy, "but not whether they had Lyme."
So, if they could not tell whether or nor anyone got Lyme disease, they could not tell whether or not LYMErix prevented it, yet they (Yale and SmithKline, and New Jersey Medical School and Connaught both reported that had 76 and 92% safe and effective vaccines anyway?
YALE’s and SMITHKLINE’s VACCINE
1: N Engl J Med. 1998 Jul 23;339(4):209-15.
Vaccination against Lyme disease with recombinant Borrelia burgdorferi outer-surface lipoprotein A with adjuvant. Lyme Disease Vaccine Study Group.
Steere AC, Sikand VK, Meurice F, Parenti DL, Fikrig E, Schoen RT, Nowakowski J, Schmid CH, Laukamp S, Buscarino C, Krause DS.
Division of Rheumatology and Immunology, Tufts University School of Medicine, New England Medical Center, Tupper Research Institute, Boston, MA 02111, USA.
BACKGROUND: The risk of acquiring Lyme disease is high in areas in which the disease is endemic, and the development of a safe and effective vaccine is therefore important. METHODS: We conducted a multicenter, double-blind, randomized trial involving 10,936 subjects who lived in areas of the United States in which Lyme disease is endemic. Participants received an injection of either recombinant Borrelia burgdorferi outer-surface lipoprotein A (OspA) with adjuvant or placebo at enrollment and 1 and 12 months later. In cases of suspected Lyme disease, culture of skin lesions, polymerase-chain-reaction testing, or serologic testing was done. Serologic testing was performed 12 and 20 months after study entry to detect asymptomatic infections. RESULTS: In the first year, after two injections, 22 subjects in the vaccine group and 43 in the placebo group contracted definite Lyme disease (P=0.009); vaccine efficacy was 49 percent (95 percent confidence interval, 15 to 69 percent). In the second year, after the third injection, 16 vaccine recipients and 66 placebo recipients contracted definite Lyme disease (P<0.001);>vaccine efficacy was 76 percent (95 percent confidence interval, 58 to 86 percent). The efficacy of the vaccine in preventing asymptomatic infection was 83 percent in the first year and 100 percent in the second year. Injection of the vaccine was associated with mild-to-moderate local or systemic reactions lasting a median of three days. CONCLUSIONS: Three injections of vaccine prevented most definite cases of Lyme disease or asymptomatic B. burgdorferi infection.
PMID: 9673298 [PubMed - indexed for MEDLINE]
1: N Engl J Med. 1998 Jul 23;339(4):216-22.
N Engl J Med 1998 Aug 20;339(8):571.
Borrelia burgdorferi outer-surface protein A to prevent Lyme disease. Recombinant Outer-Surface Protein A Lyme Disease Vaccine Study Consortium.
· Sigal LH, Zahradnik JM, Lavin P, Patella SJ, Bryant G, Haselby R, Hilton E, Kunkel M, Adler-Klein D, Doherty T, Evans J, Molloy PJ, Seidner AL, Sabetta R,
· Simon HJ, Klempner MS, Marks D, Malawista SE.
Department of Medicine, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, New Brunswick 08903-0019, USA.BACKGROUND: Lyme disease is a multisystem inflammatory disease caused by infection with the tick-borne spirochete Borrelia burgdorferi and is the most common vector-borne infection in the United States. We assessed the efficacy of a recombinant vaccine consisting of outer-surface protein A (OspA) without adjuvant in subjects at risk for Lyme disease. METHODS: For this double-blind trial, 10,305 subjects 18 years of age or older were recruited at 14 sites in areas of the United States where Lyme disease was endemic; the subjects were randomly assigned to receive either placebo (5149 subjects) or 30 microg of OspA vaccine (5156 subjects). The first two injections were administered 1 month apart, and 7515 subjects also received a booster dose at 12 months. The subjects were observed for two seasons during which the risk of transmission of Lyme disease was high. The primary end point was the number of new clinically and serologically confirmed cases of Lyme disease. RESULTS: The efficacy of the vaccine was 68 percent in the first year of the study in the entire population and 92 percent in the second year among the 3745 subjects who received the third injection. The vaccine was well tolerated. There was a higher incidence of mild, self-limited local and systemic reactions in the vaccine group, but only during the seven days after vaccination. There was no significant increase in the frequency of arthritis or neurologic events in vaccine recipients. CONCLUSIONS: In this study, OspA vaccine was safe and effective in the prevention of Lyme disease.
PMID: 9673299 [PubMed - indexed for MEDLINE]
A “92 % safe and effective vaccine” that was also unproven to prevent Lyme disease because they could not tell whether or not someone who got the vaccine also got Lyme disease, by their own admission (Sigal).
3) In the 1998 textbook, "Lyme Disease, Key Diseases Series," in the case study chapter by Yale’s Robert Schoen, in which he states that people who become ill after receiving the vaccine should not be tested with a strain of Borrelia that has the OspA-B plasmid in it (OspA, or band 31, is LYMErix),
This book was published before the FDA approved LYMErix (in Dec 1998), so Yale knew ahead of time (before FDA approved LYMErix) that they, Yale, really could not tell if LYMErix prevented Lyme (and lied to the FDA) because of the Blot-smudging or unreadable blood tests. Here, in that textbook, is Schoen saying so, in black and white.
Using a flagellin method to diagnose Lyme disease in LYMErix vaccinated people probably would not be useful due to the blot smudging, so what would be an antigen lower than 31 kilodaltons that is very indicative of Lyme? Band 23, or OspC- the antigen associated with early invasion and brain invasion.
The Problem With OspC
Borrelia burgdorferi strain B31 expresses little or no OspC and SmithKline and Yale used strain B31 to Blot people in their LYMErix trial. Practically no one got ”Lyme disease,” in Yale’s vaccine trial because if anyone had an antibody to OspC, at 23 kD (below the smudge at 31 kD) it would not show up in the blots.
So, the vaccine must have worked? No one got “Lyme disease” who got the vaccine?
THIS IS FRAUD.
In the simplest of terms, these FRAUDSTERS changed the definition of Lyme disease from a local borreliosis to that of an arthritis, only. On the FDA’s website is part of the data package I gave to the FDA committee on Jan 31, 2001.
There was much more to that data package- that is, the actual DATA I supplied to the FDA committee to support my statements, which, as anyone in BigPharma knows, this is how it is done: Obtain the data, then write the report as an overview of what the reader can expect to find as part of the datapackage for verification. Per FDA rules.
Kindly look into the matter and make an announcement to the public, since the CDC can’t be trusted.
Allen Steere and Alan Barbour are both CDC officers and both previously demonstrated and published that Lyme was a borreliosis, and they, later, as approvers of Steere’s new and bogus testing schema for Lyme disease at the 1994 Dearborn conference, said Lyme is only an inflammatory arthritis in a knee, to which a person would have a high antibody response.
Lyme can’t be both an inflammatory disease with high antibody concentration and also be a stealth bacteria:
"It's the perfect stealth bacteria," says one frustrated physician. He's talking about Borrelia burgdorferi, the bacterium that causes Lyme disease. This illness, which is often mistaken for diseases ranging from multiple sclerosis to Lupus, can inflict excruciating headaches and muscle pain, affect the brain and nervous system, attack major organs, and inflame joints.
“Computer-generated image of the OspA structure found on the B. burgdorferi bacterium. OpA is suppressed when the bacterium moves from the tick gut into mammalian blood streams.”
If OspA is suppressed in early infection, why was it made a vaccine?
Steere says “Lyme disease” is only an arthritis in a knee, and Mark Klempner says CDC says “Lyme disease” is only an arthritis in a knee, per what Steere now insists, after describing it as a relapsing fever borreliosis, initially.
Klempner at the July 2001 Rhode Island’s South County Hospital “Diseases of Summer Conference”
Answering a Questioner:
Questioner8: I just have one more question for Dr. Klempner. Um, being that there are inadequacies, inaccuracies in the testing methods, seropositivity, etc, and the surveillance criteria that you used were just that, surveillance. And the CDC recognizes that there aer so many more people that have Lyme disease who do not meet the CDCcriteria. What’s your feeling on what percentage of patients who have Lyme disease because they have not met the criteria for diagnosis?
Klempner: I, um, I think there are a number of inaccuracies in what you just said. The CDC does not recognize that there are patients who have, um, that are seropositive that don’t meet seropositive criteria. What they say, is that these are the criteria. I think what, the question, if I could reinterpret the question a little bit, is are there patients who are out there who had Lyme disease who continue to have symptoms and um, wouldn’t fall into these categories. And the question is, how do you define patients who have had Lyme disease? You’ve gotta, you’ve gotta start with some agreed upon cohort, so what are the agreed upon criteria? And what we were trying to do, since we know this was a controversial topic to start with a group of patients who no one would doubt had had Lyme disease. And that was really the point of the study. Are there other patients who fall into equivocal goups that one could say, it’s difficult to document that they had Lyme disease? Sure, but remember we were about to do a study that was very risky. Um, meaning giving people parenteral antibiotics, doing lumbar punctures, doing huge numbers of studies on these people. It was very important to start patients that everybody agreed had had acute Lyme disease. Are there lots of other people out there who say they have Lyme disease where the documentation is lacking? You know that better than I do. Of course, there are lots of people out there who says they have lots of things that you can’t document.
Questioner8: But, but according to what I’ve read is that not everyone is going to, number one, see an EM rash, um, so when you’re are using entry criteria, diagnostic criteria, that you need to have an EM rash, and d physician diagnosed…
Klemper: If you’re’re seronegative
Questioner8: Right, okay, but there are seronegative people that don’t have the initial EM rash,And if they do, they may not see it, being on the back…
Klempner: So, then how do you know what they have, that is anybody who walks in the door who says, “I don’t feel well”, with this set of symptoms. Um, that is not a group of people that I would be comfortable putting an intravenous catheter in, an LP on, doing all this very complex study. I needed to be assured that those patients had had.Lyme disease. You’re describing a group of patients who cluster by virtue of symptoms. No different from the symptom complex that was given here [previous [Fibromyalgia talk] This is a very different symptom complex, very different patient population. Very well documented Lyme disease. And I just wanted to be sure. Um, that’s where I started my talk, at that point. That is, there are a lot of people all over this world that claim to have lots of different things. But for doing studies, I think it’s very important that we cluster patients by objective findings, strict criteria.
Questioner9: (can’t hear)… you have to be careful… (can’t hear) You can’t make the assumption that people who don’t meet that criteria would respond the same way.
Klempner: I don’t agree.
So, now, if Borreliosis or Lyme borreliosis results in an infection that becomes host-adapted (does not express the same antigens in early infection as it does late in the infection), how could Klempner have been using this CDC Dearborn criteria to diagnose Late Chronic Lyme?…
Proc Natl Acad Sci U S A. 2003 Dec 23;100(26):15953-8. Epub 2003 Dec 11.
Proc Natl Acad Sci U S A. 2004 Feb 3;101(5):1426. Camaino MJ [corrected to Caimano MJ].
Borrelia burgdorferi transcriptome in the central nervous system of non-human primates.
· Narasimhan S, Caimano MJ, Liang FT, Santiago F, Laskowski M, Philipp MT, Pachner AR, Radolf JD, Fikrig E.
Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.
Neurological symptoms are common manifestations of Lyme disease; however, the paucibacillary nature of the spirochete in this environment has precluded a molecular analysis of the spirochete in the CNS. We have now adapted differential expression analysis by using a custom-amplified library (DECAL) in conjunction with Borrelia burgdorferi whole-genome and subgenome arrays to examine in vivo gene expression by B. burgdorferi in a non-human primate (NHP) model of neuroborreliosis. The expression profile of B. burgdorferi was examined in the CNS and heart of steroid-treated and immunocompetent NHPs. Eighty-six chromosomal genes and 80 plasmid-encoded genes were expressed at similar levels in the CNS and heart tissue of both immunocompetent and steroid-treated NHPs. The expression of 66 chromosomal genes and 32 plasmid-encoded genes was increased in the CNS of both immunocompetent and steroid-treated NHPs. It is likely that the expression of these genes is governed by physiological factors specific to the CNS milieu. However, 83 chromosomal and 114 plasmid-encoded genes showed contrasting expression profiles in steroid-treated and immunocompetent NHPs. The effect of dexamethasone on the immune status of the host as well as on the host metabolic pathways could contribute to these differences in the B. burgdorferi transcriptome. Results obtained herein underscore the complex interplay of host factors on B. burgdorferi gene expression in vivo. The results provide a global snapshot of the spirochetal transcriptome in the CNS and should spur the design of experiments aimed at understanding the molecular basis of neuroborreliosis.
PMID: 14671329 [PubMed - indexed for MEDLINE]
How can Lyme be a knee-only disease of the brain which does antigenic variation, but in Late Lyme disease (which Klempner says is the criteria), you can only have to have the early disease antigens that occur over time (Steere) and is also a hypersensitivity (allergy) reaction to OspA, against which there were two vaccines, but this antibody, OspA is also not adequate for diagnosis, when, as you know, specificity is specificity.
If it is specific enough to prevent Lyme disease (LYMErix), it most certainly is specific enough to diagnose, and in fact, Yale’s claim in their patent for OspA is that this is a good recombinant diagnostic antigen as well as a “vaccine.”
If FDA agrees that that all makes sense, the whole world is in bigger trouble than we thought, because this is the capitalism and democracy-spreading that we intend to force down the whole world’s throat.
Kathleen M. Dickson
23 Garden Street
Pawcatuck, CT USA 06379
Formerly, Pfizer Inc, Special Testing and Analytical Development Group, Bldg 257
(But also the “Dangerously Intelligent” “Unibomber” “Chemist” of Stonington, say the criminally insane employees of the State of Corrupticut.)