ILADS & LDA KILLED THE CRICKETS

By Beaux Reliosis on July 26, 2015 • ( 1 )

Do you hear that?

No? Listen really, really hard.

Still don’t hear it?

Maybe you’re not listening for the right thing.

Maybe you weren’t expecting the chirp of crickets when UC Davis released its findings on Suppression of Long-Lived Humoral Immunity Following Borrelia burgdorferi Infection.

http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1004976

Crickets.

Do you hear them now? No? Oh, they must be as bewildered as I am that neither ILADS nor LDA have commented on this UNBELIEVABLY IMPORTANT study which was released nearly a MONTH AGO. (Great job, guys. You stupefied the crickets. Maybe it’s a new syndrome for the insect DSM–crickets stunned into complete and utter silence.)

I will do ILADS and LDA a favor and first of all, thank the research team of Rebecca A. Elsner, Christine J. Hastey, Kimberly J. Olsen and Nicole Baumgarth, on behalf of all of us who are either fighting Lyme disease or advocating in some way for those who suffer. (Shame on you, ILADS and LDA; you seem to have forgotten your manners.) IDSA is probably working away figuring out how to get the article retracted, but we expect that from those criminal types, so gratitude from that crew for something like this would be akin to all of them quietly lining up for their mugshots, prison garb and shackles. Not gonna happen.

Anyway, I do want to thank these courageous women scientists–yes, women, who will save the world–for confirming what our LYMErix whistleblower has been saying for 16 years: that Lyme is a disease of immunosuppression and B-cell incompetence, and that it also messes up the response to viruses.

“Infections with the Lyme Disease agent, Borrelia burgdorferi, often fail to generate long-term protective immunity. We show here that this is because the immune system of the Borrelia-infected host generates only short-lived, structurally abnormal and non-functional germinal centers. These germinal centers fail to induce memory B cells and long-lived antibody-producing plasma cells, leaving the host susceptible to reinfection with Bb. This inability to induce long-term immunity was not due to the nature of Borrelia antigens, as even T-dependent antigens of Borrelia were unable to induce such responses. Moreover, influenza vaccine antigens, when applied during Borrelia-infection, failed to induce strong antibody responses and immune-protection from influenza challenge. This data illustrate the potent, if temporal, immune suppression induced by Borrelia-infection. Collectively, the data reveal a new mechanism by which B. burgdorferi subverts the adaptive immune response.”

What’s even better: this is not new news. This is confirmation and reconfirmation and re-reconfirmation of past studies by the likes of Clifford Harding, the NIH and the crooks themselves.

1. Here are Martin & Marques of NINDS (NIH) saying OspA (TLR2/1 agonist) is responsible for the humoral immunosuppression with chronic encephalitis we know of as NeuroLyme:

http://www.ncbi.nlm.nih.gov/pubmed/16783164

“…In contrast, a large number of HLA-related molecules were repressed at both the RNA and the protein levels in stimulated monocytes, whereas secretion of IL-10 and TNF-alpha was strongly induced. These results show that signaling through TLR1/2 in response to B. burgdorferi can elicit opposite immunoregulatory effects in blood and in brain immune cells, which could play a role in the different susceptibility of these compartments to infection.”

2. Here is Paul Duray, NASA/NIH/NIC/US Army Top Pathologist, in 1992: “In Chronic Lyme victims’ cerebrospinal fluid, I see what look like Epstein-Barr transformed lymphocytes.”

Image courtesy of http://www.actionlyme.org

3. Look at anything Clifford Harding says about TLR2/1 agonists:

http://www.ncbi.nlm.nih.gov/pubmed/?term=Harding%2C+Clifford+V%5BAuthor%5D

4. Raymond Dattwyler, Cryminal Extraordinaire:

Modulation of natural killer cell activity by Borrelia burgdorferi.

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.

Image courtesy of http://www.actionlyme.org

(See more at http://www.actionlyme.org/DATTWYLER_NK_SUPPRESSION.htm, since PubMed has wiped the actual article text from its records.)

5. Dave Persing explained why the original Osps should not be used as vaccines:

“Accordingly, the methods of the invention provide a powerful and selective approach for modulating the innate immune response pathways in animals without giving rise to the toxicities often associated with the native bacterial components that normally stimulate those pathways.”

Courtesy of http://www.actionlyme.org/STEALTH_DISABLERS.htm

…And he patented it. For more on the patents, visit my sister site, www.ohioactionlyme.org or check out the complete Charge Sheets.

I could go on and on, but I’m very tired from a recent crash of my own. So, I’m going to wrap this up. Where does this leave us?

Everybody agrees that Lyme disease is about immunosuppression, incompetent B-cells, reactivated herpesviruses and opportunistic infections. Sounds an awful lot like AIDS, doesn’t it? I guess what ILADS and LDA are telling us, through their complete silence, is that they don’t want the world to realize that they have been wrong all along—treating an AIDS-like disease with buttloads of antibiotics. Talking about attacking biofilms and coinfections, one by one, in an excruciatingly long process. Raking in big bucks for big salaries—uh, I mean lots of research. Bankrupting patients so they’re SOL when the relapse hits. Pushing Lyme bills to protect the doctors who are bankrupting patients. Obstruct, delay, divert.

Guess what, guys? The research has been pretty conclusive for at least 15 years. Now UC Davis has confirmed it, once again. And the very people who should be screaming about it from every rooftop and demanding justice for us Lymies are DEAD SILENT.

Can you hear the crickets? Yeah, me neither.

WHO WILL HEAR US?