Spirochetes Cause An Acquired Immune Deficiency Disease, Also Known As AIDS

“It used to be called Lyme relapsing fever or Lyme borreliosis, and historically, spirochetal diseases are incurable and devastating – not to mention chronic or a permanent disability – but “Lyme disease?”  That’s something that happened in the minds of people who would not be able to earn royalties from this new DNA technology and the Bayh-Dole Act, where people can OWN DNA and therefore OWN diseases, UNLESS THEY LIED ABOUT IT, and acted like spirochetes were just regular bacteria and not their own ancient phylum, and shedder of triacyl lipoproteins or FUNGAL ENDOTOXINS!!”

https://crymedisease.wordpress.com/2016/08/02/inhibition-of-apoptosis/

 

OspA is Pam3Cys.  Spirochetes cause an Acquired Immune Deficiency (AIDS).  Just like the sky is unchangeably blue, these are the facts.

Pam3Cys is an endotoxin managed by TLR 2/1, which makes it fungal-like.  It causes immunosuppression.  It is a triacylated lipoprotein.  It may be one of the most politicized molecules on the planet at this point.

pam3cys image

 

You can literally buy Pam3Cys to cause experimental sepsis and study immune suppression.  But “The Cabal” said that it was a vaccine for Lyme disease.  Isn’t that silly?  Maybe we would be laughing if people weren’t being tortured to death and dying of starvation alone in the woods.  Fungal diseases have been known since forever to be very serious and long lasting, even fatal.

Beaux_PoopToxinMeme.jpg

 

This is much worse than a chronic bacterial infection.  Yes, spirochetes persist.  But spirochetes drilling through tissues is not what keeps people sick.  Spirochetes shed their blebs and those are covered in outer surface proteins (Osp’s).  These Osp’s are fungal-like antigens that cause immunological meltdown.  Even if you could kill spirochetes the irreversible damage to the immune system is done within 10 days.

playdoh_spiro

“Many researchers believe that the secret to B. burgdorferi‘s infectivity and inflammatory capacity lies in the interaction of its surface proteins with the host’s immunological system. Yale researcher Stephen Barthold, a veterinarian and professor of comparative medicine who developed the first mouse model of Lyme disease, studies the expression of B. burgdorferi surface proteins throughout various stages of the spirochete’s life cycle. He finds that during the early stages of infection, B. burgdorferi avoids immune detection by decreasing its expression of surface proteins or cloaking its expressed surface proteins under a layer of slime. “It’s using some sort of stealth-bomber-type mechanism,” he says. Or, using another diversionary tactic called blebbing, the spirochete can pinch off bits of its membrane in order to release its surface proteins. Explains Barbour: “It’s like a bacterial Star Wars defense program,” in which released surface proteins might intercept incoming host antibodies, keeping the spirochete safe from immunological attack.”        

https://www.the-scientist.com/?articles.view/articleNo/17985/title/Researchers-Finding-Rewarding-Careers-As-Software-Entrepreneurs/

This is from Alan Barbour, who owns about a million patents on Borrelia Burgdorferi and is currently on the scientific advisory board for the Bay Area Lyme Disease Foundation.  ​

 

So you get bit by an infected tick and it regurgitates spirochetes into you.  Here is the simplest explainer on what happens next:

“Spirochetes disseminate to the lymph nodes, bone marrow, spleen and brain within a week of infection (1). Lymph node germinal centers, where B cells are supposed to mature and be assigned an immune system function, are rendered incompetent (2). Meanwhile, the toxic triacyl lipoproteins that are shed by spirochetes on blebs of their outer surface get to work causing tolerance and cross tolerance (2,3,4), AKA shutting down the immune system (5,6). There is generalized immune suppression at the same time there are brain inflammation and neurologic complications (7,8,9,10). Opportunistic infections take hold and herpesviruses reactivate (11,12). Half the cases don’t recover fully, regardless of treatment (13,14,15). The outcome is cancer-like (16,17).”

https://badlymeattitude.com/2017/12/13/this-is-lyme/

 

Zombie_Meme

 

 

Then, we have the whole inhibition of apoptosis crisis.

Apoptosis is the auto-kill mechanism.  A cell is supposed to commit suicide when it knows that it’s infected.

Both OspA and EBV inhibit this very important process.

Both spirochetes and EBV like to hang out in the lymph nodes.

 

 

Spirochetes are way outnumbered by the blebs as you can see in the graphic below.

OspA with data2

The LYMErix vaccine caused the same disease we know as “Chronic Lyme” without spirochetes.  You don’t even need whole spirochetes to cause this disease.  That is why trying to kill them does not get anyone better.  HALF the cases fail even early treatment.  So this isn’t about spirochetes, just like the sky is not green.

It is the fungal-like antigens, that are endotoxins, causing immune suppression and tolerance and inhibiting apoptosis that allows opportunistic infections to flourish and latent viruses to reactivate.  That is what is causing the shit show of symptoms we all have.  We all have post sepsis syndrome.  B cell AIDS.  Pseudolymphoma.  Lyme-phoma.  Cancer-like.

b cells quite atypical    lyme psuedo lymphoma

Duray cancer:lyme.png

 

 

 

 

 

 

 

 

 

“These look like EBV transformed cells.”  Yep, that’s exactly what this is about.

“On occasion, these atypical-appearing large lymphocytes have been misinterpreted in biopsy by several laboratories as cells of a malignant lymphoma or leukemia.  Bb antigens, then, may stimulate growth of immature lymphocytic suibsets in some target organs, as well as in the cerebrospinal fluid (Szyfelbein and Ross 1988).  Usual bacterial infections do not produce such lymphocytic infiltrates in tissue.  These immunoblastoid cells in Bb infections at times resemble those found in Epstein-Barr virus infections.  Does Bb reactivate latent virus infections in tissues?  Do some tick inocula harbor simultaneous infectious agents (ixodid ticks can harbor Rickettsiae, Babesia microti, and Ehrlichia bacteria, in addition to Bb), producing multi-agent infections in some hosts?  Further studies can clarify these issues by mans of tissue-based molecular probe analysis.” –
Paul Duray, NCI, NIH, Ft. Detrick, at the 1992 Cold Spring Harbor Crooks’ Conference, published in Steve Schutzer’s Lyme Disease: Molecular and Immunologic Approaches.

 

If LYMErix caused the same disease, then what is the disease?

If OspA alone causes the same chronic, multi-system, protean disease…

….it means that this isn’t about the spirochetes.  It only starts with them.

 

Yes, spirochetes persist.  But that’s not what “they” are afraid of everyone finding out.  “They” are literally terrified of us, their victims, knowing that OspA is Pam3Cys because it exposes the entire FRAUD CRIME.  This crime is a Racketeer Influenced Corrupt Organization (RICO) charge, and those carry life sentences.  The truth is in their own patents and in their own words.  This is not mysterious, it has been known since at least 1986 what this disease is.

There is no controversy, only crime.  The disease IS the crime.  The crime IS the disease.  Literally.  

Both the testing and the case definition of Lyme disease were fraudulently changed.  See TruthCures.org for more information.  Watch the free documentary on YouTube “LYME CRYME”.  The DOJ needs to do their job and prosecute the CRYME, the complaint was filed in 2003.

WESTERN_BLOT_TCvERSION

 


References:
1. Lymphoadenopathy during Lyme Borreliosis Is Caused by Spirochete Migration-Induced Specific B Cell Activation Stefan S. Tunev1,2¤, Christine J. Hastey1,4, Emir Hodzic1, Sunlian Feng1, Stephen W. Barthold, Nicole Baumgarth
2. Suppression of Long-Lived Humoral Immunity Following Borrelia burgdorferi Infection Rebecca A. Elsner, Christine J. Hastey, Kimberly J. Olsen, Nicole Baumgarth Published: July 2, 2015
3. J Infect Dis. 2006 Mar 15;193(6):849-59. Epub 2006 Feb 8. Borrelia burgdorferi lipoprotein-mediated TLR2 stimulation causes the down-regulation of TLR5 in human monocytes. Cabral ES1, Gelderblom H, Hornung RL, Munson PJ, Martin R, Marques AR.
4. Borrelia burgdorferi-Induced Tolerance as a Model of Persistence via Immunosuppression
Isabel Diterich1, Carolin Rauter1, Carsten J. Kirschning2 and Thomas Hartung1,*
5. Lyme Cabal members Gary Wormser and Allen Steere – and even the “CDC officer” Paul Mead – finally admit Late Lyme and LYMErix diseases are immunosuppression outcomes; say “TLR2/1 agonism” (immunosuppression) is probably the “more important” driver of the disease outcome. Nat Rev Dis Primers. 2016 Dec 15;2:16090. doi: 10.1038/nrdp.2016.90. Lyme borreliosis. Steere AC1,2, Strle F3, Wormser GP4, Hu LT5, Branda JA6, Hovius JW7, Li X8, Mead PS9.
6. Seronegative Lyme disease. Dissociation of specific T- and B-lymphocyte responses to Borrelia burgdorferi.
Dattwyler RJ1, Volkman DJ, Luft BJ, Halperin JJ, Thomas J, Golightly MG.
N Engl J Med. 1988 Dec 1;319(22):1441-6.
7. Latov, N., Wu, A. T., Chin, R. L., Sander, H. W., Alaedini, A. and Brannagan, T. H. (2004), Neuropathy and cognitive impairment following vaccination with the OspA protein of Borrelia burgdorferi. Journal of the Peripheral Nervous System, 9: 165–167. doi:10.1111/j.1085-9489.2004.09306.x
8. Neurological complications of vaccination with outer surface protein A (OspA). Marks DH1. Int J Risk Saf Med. 2011;23(2):89-96. doi: 10.3233/JRS-2011-0527
9. J Neuropathol Exp Neurol. 2006 Jun;65(6):540-8. Borrelia burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral blood monocytes but differentially regulates HLA-class II expression.
“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.”
10. Parthasarathy G, Philipp MT. Receptor tyrosine kinases play a significant role in human oligodendrocyte inflammation and cell death associated with the Lyme disease bacterium Borrelia burgdorferi. Journal of Neuroinflammation. 2017;14:110. doi:10.1186/s12974-017-0883-9.
11. Hutchins NA, Unsinger J, Hotchkiss RS, Ayala A. The new normal: immuno-modulatory agents against sepsis immune suppression. Trends in molecular medicine. 2014;20(4):224-233. doi:10.1016/j.molmed.2014.01.002.
12. Walton AH, Muenzer JT, Rasche D, Boomer JS, Sato B, et al. (2014) Reactivation of Multiple Viruses in Patients with Sepsis. PLoS ONE 9(6): e98819. doi:10. 1371/journal.pone.0098819
13. The Clinical Spectrum and Treatment of Lyme Disease
ALLEN C. STEERE, M.D., STEPHEN E. MALAWISTA, M.D., NICHOLAS H. BARTENHAGEN, M.D., PHYLLIS N. SPIELER, M.D., JAMES H. NEWMAN, M.D., DANIEL W. RAHN, M.D., GORDON J.HUTCHINSON, M.D., JERRY GREEN, M.D., DAVID R. SNYDMAN, M.D., AND ELISE TAYLOR, B.A
THE YALE JOURNAL OF BIOLOGY AND MEDICINE 57(1984),453-461
14. Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1518-25.
A perspective on the treatment of Lyme borreliosis.
Luft BJ1, Gorevic PD, Halperin JJ, Volkman DJ, Dattwyler RJ.
15. Bouquet J, Soloski MJ, Swei A, Cheadle C, Federman S, Billaud J-N, Rebman AW, Kabre B, Halpert R, Boorgula M, Aucott JN, Chiu CY. 2016. Longitudinal transcriptome analysis reveals a sustained differential gene expression signature in patients treated for acute Lyme disease. mBio 7(1):e00100-16. doi:10.1128/mBio.00100-16.
16. Clinical Pathologic Correlations of Lyme Disease by Stage
PAUL H. DURAY
Department of Pathology
Fox Chase Cancer Center Philadelphia, Pennsylvania 191 I I
ALLEN C. STEERE
Department of Internal Medicine Division of Rheumatology Tufts University School of Medicine Boston, Massachusetts 02111
17. The Clinical Spectrum and Treatment of Lyme Disease
ALLEN C. STEERE, M.D., STEPHEN E. MALAWISTA, M.D., NICHOLAS H. BARTENHAGEN, M.D., PHYLLIS N. SPIELER, M.D., JAMES H. NEWMAN, M.D., DANIEL W. RAHN, M.D., GORDON J.HUTCHINSON, M.D., JERRY GREEN, M.D., DAVID R. SNYDMAN, M.D., AND ELISE TAYLOR, B.A. THE YALE JOURNAL OF BIOLOGY AND MEDICINE 57(1984),453-461
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