Mutated B-Cells Resemble Lymphoma or Leukemia in Lyme and LYMErix Victims

Allen Steere, the psychopath who says you can only have Lyme if you're not sick, went to Europe in 1992-1993 to commit research fraud by falsifying Lyme disease testing to exclude all neurologic Lyme / LYMErix victims from the testing making the sickest most disabled patients on the planet undetectable for the later monopoly on vector borne disease test kits after the LYMErix vaccine was on the market. He raised the bar to a high antibody concentration by adding the ELISA when in fact, Lyme and LYMErix victims produce no to little antibodies. Steere also dropped OspA and B from the diagnostics, in which prior he said were the most prominent antibodies. 

In 1988, prior
 to Steere's research fraud stunt, he published that B-cells are mutated and it resembles Lymphoma or Leukemia with chronic active Epstein-Barr, an AIDS like post-sepsis illness in the victims who he claims aren't even sick, they're all crazy psych or Munchhausen's patients catching Hypochondria from ticks. 

Reference: Pam3Cys is
 OspA = outer surface protein shed via Borrelia spirochetes or injected LYMErix vaccine antigen. A highly toxic immune suppressing endotoxin inhibiting apoptosis or renders b-cells incompetent. 

Clinical pathologic correlations of Lyme disease by stage.

Duray PH1Steere AC.
 The plasma cell precursors are large, appear tumor-like, and can resemble ***Reed-Sternberg cells.*** Others look like typical immunoblasts (FIG. 1). In one example, cervical lymph nodes show cell degeneration with karyorrhexis and nuclear debris of lymphoid elements. This patient had repeated high fevers and marked discomfort of neck nodes. Large atypical immunoblasts can also be seen in the spleen and bone marrow. The red pulp of the spleen is congested, not unlike that seen in infectious mononucleosis. Spirochetes can be demonstrated in the lymph nodes, spleen and bone marrow and liver. There is a transient hepatitis reflected by elevated liver cell enzymes such as SGOT, SGPT, and GGT. The liver can vary from a mild lymphocytic portal triaditis all the way to liver cell derangement that simulates acute viral hepatitis. The cells at this stage appear swollen with clear cytoplasm and microvesicles of fat (FIG. 2). Numerous leukocytes are seen in the sinusoids, and there is Kupffer cell hyperplasia…”

 Paul Duray, NCI, NIH, Ft. Detrick
"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."

Lymphoadenopathy during lyme borreliosis is caused by spirochete migration-induced specific B cell activation.

 "Together, these findings suggest a novel evasion strategy for B. burgdorferi: subversion of the quality of a strongly induced, potentially protective borrelia-specific antibody response via B. burdorferi's accumulation in lymph nodes."

Nicole Baumgarth in 2015 saying B-cell germinal centers collapse resulting in the inability to then fight off viral infections, like AIDS. 

Suppression of Long-Lived Humoral Immunity Following Borrelia burgdorferi Infection

“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 Bburgdorferi subverts the adaptive immune response.”

Role of TLR in B cell development: signaling through TLR4 promotes B cell maturation and is inhibited by TLR2 

The role of TLR4 in mature B cell activation is well characterized. However, little is known about TLR4 role in B cell development. Here, we analyzed the effects of TLR4 and TLR2 agonists on B cell development using an in vitro model of B cell maturation. Highly purified B220(+)IgM(-) B cell precursors from normal C57BL/6 mouse were cultured for 72 h, and B cell maturation in the presence of the TLR agonists was evaluated by expression of IgM, IgD, CD23, and AA4. The addition of LPS or lipid A resulted in a marked increase in the percentage of CD23(+) B cells, while Pam3Cys had no effect alone, but inhibited the increase of CD23(+) B cell population induced by lipid A or LPS. The TLR4-induced expression of CD23 is not accompanied by full activation of the lymphocyte, as suggested by the absence of activation Ag CD69. Experiments with TLR2-knockout mice confirmed that the inhibitory effects of Pam3Cys depend on the expression of TLR2. We studied the effects of TLR-agonists on early steps of B cell differentiation by analyzing IL-7 responsiveness and phenotype of early B cell precursors: we found that both lipid A and Pam3Cys impaired IL-7-dependent proliferation; however, while lipid A up-regulates B220 surface marker, consistent with a more mature phenotype of the IgM(-) precursors, Pam3Cys keeps the precursors on a more immature stage. Taken together, our results suggest that TLR4 signaling favors B lymphocyte maturation, whereas TLR2 arrests/retards that process, ascribing new roles for TLRs in B cell physiology.

Lyme victims are walking cesspool's of disease with global immunosuppression but inflammation in the brain. B-cells are mutated and as Steere said before his intended profitable stunt, it resembles Lymphoma or Leukemia with chronic active Epstein-Barr in those who he says are not even sick, they're just crazy loonies who need a psychiatrist. We are partially to blame for this medical holocaust to humanity as we continue the same path allowing fake non-profits and ILADS to take over the show and be our voice as they refuse to talk about the crime and the real disease mechanism, they swooped right in and created a monopoly to profit off the severely disabled and destitute. Lyme victims are victims of prosecutable heinous crimesgenocide and straight up murder  perpetrated by CDC criminals and their wealthy backers for profit and greed. If the LYMErix vaccine caused the same disease, what is the disease? Why won't any of these non-profits talk about it? They would lose their free money and glory. 25 years later they continue feeding desperate disabled victims false hope.


  1. We will fight for humanity. For or childeren for there future. Everyone have right to live a normal life.

  2. Thanks for this explainer, excellent.

  3. Yes we need someone to push for the prosecution of these criminals. That, however, does take away from the fact that there are still people who need help in the meantime. I am a pissed off husband of a Lymie, I will see justice for my wife. I will bring it to those who have laughed scoffed and called her crazy. But while I pursue justice I hope to provide peace for those I can. We need these groups and the relief they bring. War torn countries need the Red Cross just as much as they do the troops of an allies army.

  4. Meanwhile, the new OspA trials are running,


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