Link to the report with the featured imagine, above:
This short explainer shows how Lyme disease causes LYMErix disease or post-sepsis syndrome, with, eventually, the reactivated latent viral infections that are the REAL “Imitators” or actually, cause-ers.
See more by NIH’s Marques, Martin, and Duray on the Occam’s Razor report. They say the likes of OspA is responsible for the generalized immunosuppression, chronic brain inflammation, “these look like Epstein-Barr transformed cells,” and in the New York Times Marques straight up said “Epstein-Barr could be the real culprit”:
Edward McSweegan http://rel-risk.blogspot.com/ and Durland Fish (chronic troll) are 24/7 FRANTIC that you might discover how this works, because it cross-applies to other failed vaccines. Kids are getting the viruses and not the protection from vaccines. The US Govt should not have picked psychopaths to manage this probable accidental release. The press has never published the true story of Lyme. ILADS for the most part are low class people and don’t actually care what is the right or wrong thing to do, and are not curing people. They’re not even helping people because rather than say “Lyme causes sepsis and post sepsis syndrome” and help you get Disability, they say they can cure you or help improve your life. Were that true, we would not be having this discussion. (“After 15 years we have nothing,” from ILADS.)
An NIH patent, explaining how Lyme causes LYMErix-disease (this also became the Igenex LUAT):
“The invention relates to novel antigens associated with Borrelia burgdorferi which are exported (or shed) in vivo and whose detection is a means of diagnosing Lyme disease. The antigens are extracellular membrane vesicles and other bioproducts including the major extracellular protein antigen. Another object of the invention is to provide antibodies, monoclonal and/or polyclonal, labeled and/or unlabeled, that are raised against the antigens. A further object of the invention is to provide a method of diagnosing Lyme disease by detecting the antigens in a biological sample taken from a host using the antibodies in conventional immunoassay formats. Another object of the invention is to provide kits, for the diagnosis of Lyme disease, comprising the antibodies and ancillary reagents. The advantage of the antibodies used in the invention is that they react with the antigens from geographically diverse strains of Borrelia burgdorferi, but do not react with antigens from related Borrelia spirochetes.”
Characterization of multiprotein complexes of the Borrelia burgdorferi outer membrane vesicles.
“Although we uncovered the existence of at least 10 distinct OM complexes harboring several unique subunits, the complexome is dominated by the frequent occurrence of a limited diversity of membrane proteins, most notably P13, outer surface protein (Osp) A, -B, -C, and -D and Lp6.6.”
See where NIH’s Martin and Marques say these OspA-ish molecules are responsible for humoral immunosuppression with chronic brain inflammation:
“Bacterial lipoproteins can disseminate from the periphery to inflame the brain.”
“The current view is that bacteria need to enter the brain to cause inflammation. However, in mice infected with the spirochete Borrelia turicatae, we observed widespread cerebral inflammation despite a paucity of spirochetes in the brain parenchyma at times of high bacteremia. Here we studied the possibility that bacterial lipoproteins may be capable of disseminating from the periphery across the blood-brain barrier to inflame the brain. For this we injected normal and infected mice intraperitoneally with lanthanide-labeled variable outer membrane lipoproteins of B. turicatae and measured their localization in blood, various peripheral organs, and whole and capillary-depleted brain protein extracts at various times. Lanthanide-labeled nonlipidated lipoproteins of B. turicatae and mouse albumin were used as controls. Brain inflammation was measured by TaqMan RT-PCR amplification of genes known to be up-regulated in response to borrelial infection. The results showed that the two lipoproteins we studied, LVsp1 and LVsp2, were capable of inflaming the brain after intraperitoneal injection to different degrees: LVsp1 was better than LVsp2 and Bt1 spirochetes at moving from blood to brain. The dissemination of LVsp1 from the periphery to the brain occurred under normal conditions and significantly increased with infection. In contrast, LVsp2 disseminated better to peripheral organs. We conclude that some bacterial lipoproteins can disseminate from the periphery to inflame the brain.”
“Specific adherence of Borrelia burgdorferi extracellular vesicles to human endothelial cells in culture.”
“Borrelia burgdorferi produces extracellular vesicles which contain some of the outer surface proteins of the bacterium (e.g., OspA and OspB). Borrelial vesicles, isolated by differential centrifugation and filtration, were tested for the ability to bind to cultured human umbilical vein endothelial (HUVE) cells in culture. The recently described lipoprotein OspD was expressed on vesicles. Vesicles exhibited differential expression of OspB and OspD in a relationship with passage number and medium serum supplement type, respectively. Qualitative immunoblotting analyses demonstrated dose-dependent, passage number-dependent adsorption of vesicles by HUVE cells. This adsorption was demonstrated to be dependent upon a borrelial component of the vesicle and not due to the presence of minor contamination with intact spirochetes. Quantitative experiments examining inhibition of B. burgdorferi-HUVE association as a function of prior vesicle-HUVE association demonstrated dependence upon (i) a borrelial component(s) in the vesicle, (ii) low passage number, and (iii) vesicle protein concentration. However, vesicle pretreatment of the HUVE cell monolayer was not requisite for this inhibition. Vesicles from highly passaged borrelias were noninhibitory for B. burgdorferi-HUVE cell association, regardless of the serum used to supplement the medium. The use of vesicles as a tool for studying B. burgdorferi pathogenesis and/or physiology is proposed.”
So, Lyme disease is the same thing as LYMErix disease. The OspA vaccine gave people the same disease (see the Occam’s Razor for those quotes and proofs) we know of as “Chronic Lyme” because “Chronic Lyme” is really post-sepsis syndrome. We can’t help you unless you try to help yourself and understand that “Lyme disease” is not about spirochetes as shown here and as shown by LYMErix disease. It STARTS with spirochetes, but mainly ends with mutated B cells and an AIDS-like disease.
Today is March 9, 2016. I have spent the three days thinking what would be the IN YOUR FACE thing to say to you (see the feature image) to make you all understand that none of the non-nonprofits or anyone in ILADS and especially no one at IDSociety.org (they’re usually even dumber and less educated than ILADS) is capable of reading the science independently and seeing for themselves what is true.
All the rest of MD-America never even wonders why there is a dispute over the chronicity of Lyme. They don’t even know what a spirochete is. Spirochetes are their own phylum, ancient, not bacteria, not evolutionarily related to any other organisms, are parasites, and Borrelia, especially, do not form colonies in vivo.
Also, tick borne diseases (TBDs) are nearly all fungal antigen-bearers and cause the same immunosuppression. Due to global warming, TBDs have moved from mainly Africa to the northern hemisphere and humans do not have much immunity to them, no matter how long removed from Africa, evolutionarily.
“Spirochetes are nasty,” said one PhD Chemist at Pfizer, to me.