This is the simplest explanation I’ve come up with, so far. Go ahead and print this for anyone who needs to know. Tell them #truthcureslyme.
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).
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
Categories: Lyme Disease