Post by Admin/ Traveler on Nov 25, 2017 20:34:03 GMT
This is a blog post from another Lyme patient that I am proud to know. I will copy and paste the entire blog post below, so you can read it in it's entirety. We not only need to be outraged, but outraged enough to help get him removed from this working group!! I'm just livid that this "man" (he's got to be soul-less to do the things he's done and then to accept this!).
Gary Wormser got a seat on the HHS Tick Borne Disease Working Group
Posted on November 25, 2017 by LYMECRYME
Are you as flabbergasted as I am with who has been chosen to be in the new HHS Working Group for Tick Borne Disease? If you object to this obvious conflict of interest please send an email to the Director of the Working Group, Dr. Wiltoski, and let him know that we would like Wormy removed. tickbornedisease@hhs.gov
Let’s take a look at the work of one of the lead authors of the IDSA Guidelines, Gary Wormser. This man is a criminal, let’s shed some light on his crimes against humanity. If he knows that OspA causes immunosuppression then he knows that OspA could never have been a vaccine 😉
2000: “The magnitude of modulation was directly dependent on the quantity of OspA.” Here is saying the amount of OspA you get, whether it’s injected by syringe or tick bite, determines how significant the immune suppression you get will be.
“OspA interferes with the response of lymphocytes to proliferative stimuli including a blocking of cell cycle phase progression.”
“We have previously demonstrated that proteins of B. burgdorferi are capable of modulating human cellular immune responses [7]. Suppression of in vitro mitogen- or antigen-mediated proliferative responses of lymphocytes and reduced production of interleukin-2 (IL-2) from lymphocytes were demonstrated using protein extracts of B. burgdorferi. These early studies were confirmed by a report of de Souza et al. [8], who observed that B. burgdorferi infection in mice resulted in impaired T and B cell proliferation to mitogens and reduced IL-2 and IL-4 production. The nature of the B. burgdorferi proteins responsible for suppression of cellular immunity has not been defined. In this study we examined the modulating activity of a recombinant outer surface protein A (OspA) vaccine preparation on cellular immune responses.”
Modulation of lymphocyte proliferative responses by a canine Lyme disease vaccine of recombinant outer surface protein A (OspA)
2005: Wormser describing the two types of “Lyme disease”, HLA (lots of antibodies) and HLA-restricted (low or no antibodies). Here we can see that he knows that two types exist, which means he knows that 85% of cases are being missed on testing and subsequently tortured.
A Case Study To Examine HLA Haplotype Associations in Patients With Posttreatment Chronic Lyme disease.
A Case-Control Study to Examine HLA Haplotype Associations in Patients with Posttreatment Chronic Lyme Disease
2012: Spirochetes cause immune suppression or Post Sepsis Syndrome.
“During natural infection, initiation of the host response begins with CD14 recognition of triacylated borrelial lipoproteins and subsequent activation of TLR-2 in partnership with TLR-1. Such bacterial recognition activates the NF-κB, phosphatidylinositol 3-kinase/Akt, and p38 MAPK pathways. The ensuing signaling cascades initiate inflammation-associated gene activities responsible for host defense, as well as negative regulatory pathways intended to mitigate the severity and duration of the inflammatory response to spirochetes. The latter goal is achieved, in part, through the action of p38 MAPK–induced suppressors of cytokine signaling (SOCS), which down-regulate inflammation by targeting various points in the NF-κB pathway.”
The Toll of a TLR1 polymorphism in Lyme disease: A tale of mice and men
“This finding suggests that there is redundancy in the ability of the innate immune system to recognize B. burgdorferi and/or that these components can activate pathways that produce anti-inflammatory cytokines, … – the anti-inflammatory effects might be the more important function of TLR signaling.”
Lyme borreliosis
1994: IMPORTANT! At the Dearborn Conference (where they changed the definition of “Lyme disease” to mean just arthritis in a knee) Wormser reported that Steeres blotting method was only detecting 15% of cases.
“Overall, 51 of 59 (86%) convalescent phase serum specimens were reactive by IB [Dearborn criteria Immunoblot-KMD], 35 of which were interpreted as positive; 26 based on IgM criteria, 8 based on both IgM and IgG, and 1 based on IgG criteria…”
Serodiagnosis in Early Lyme disease
Here are some links with some detailed chronology of the crime:
The Conspirators, they own the patents and changed the testing
Cryme time line
As anyone can see, this man belongs in prison, not in the Working Group.
Gary Wormser got a seat on the HHS Tick Borne Disease Working Group
Posted on November 25, 2017 by LYMECRYME
Are you as flabbergasted as I am with who has been chosen to be in the new HHS Working Group for Tick Borne Disease? If you object to this obvious conflict of interest please send an email to the Director of the Working Group, Dr. Wiltoski, and let him know that we would like Wormy removed. tickbornedisease@hhs.gov
Let’s take a look at the work of one of the lead authors of the IDSA Guidelines, Gary Wormser. This man is a criminal, let’s shed some light on his crimes against humanity. If he knows that OspA causes immunosuppression then he knows that OspA could never have been a vaccine 😉
2000: “The magnitude of modulation was directly dependent on the quantity of OspA.” Here is saying the amount of OspA you get, whether it’s injected by syringe or tick bite, determines how significant the immune suppression you get will be.
“OspA interferes with the response of lymphocytes to proliferative stimuli including a blocking of cell cycle phase progression.”
“We have previously demonstrated that proteins of B. burgdorferi are capable of modulating human cellular immune responses [7]. Suppression of in vitro mitogen- or antigen-mediated proliferative responses of lymphocytes and reduced production of interleukin-2 (IL-2) from lymphocytes were demonstrated using protein extracts of B. burgdorferi. These early studies were confirmed by a report of de Souza et al. [8], who observed that B. burgdorferi infection in mice resulted in impaired T and B cell proliferation to mitogens and reduced IL-2 and IL-4 production. The nature of the B. burgdorferi proteins responsible for suppression of cellular immunity has not been defined. In this study we examined the modulating activity of a recombinant outer surface protein A (OspA) vaccine preparation on cellular immune responses.”
Modulation of lymphocyte proliferative responses by a canine Lyme disease vaccine of recombinant outer surface protein A (OspA)
2005: Wormser describing the two types of “Lyme disease”, HLA (lots of antibodies) and HLA-restricted (low or no antibodies). Here we can see that he knows that two types exist, which means he knows that 85% of cases are being missed on testing and subsequently tortured.
A Case Study To Examine HLA Haplotype Associations in Patients With Posttreatment Chronic Lyme disease.
A Case-Control Study to Examine HLA Haplotype Associations in Patients with Posttreatment Chronic Lyme Disease
2012: Spirochetes cause immune suppression or Post Sepsis Syndrome.
“During natural infection, initiation of the host response begins with CD14 recognition of triacylated borrelial lipoproteins and subsequent activation of TLR-2 in partnership with TLR-1. Such bacterial recognition activates the NF-κB, phosphatidylinositol 3-kinase/Akt, and p38 MAPK pathways. The ensuing signaling cascades initiate inflammation-associated gene activities responsible for host defense, as well as negative regulatory pathways intended to mitigate the severity and duration of the inflammatory response to spirochetes. The latter goal is achieved, in part, through the action of p38 MAPK–induced suppressors of cytokine signaling (SOCS), which down-regulate inflammation by targeting various points in the NF-κB pathway.”
The Toll of a TLR1 polymorphism in Lyme disease: A tale of mice and men
“This finding suggests that there is redundancy in the ability of the innate immune system to recognize B. burgdorferi and/or that these components can activate pathways that produce anti-inflammatory cytokines, … – the anti-inflammatory effects might be the more important function of TLR signaling.”
Lyme borreliosis
1994: IMPORTANT! At the Dearborn Conference (where they changed the definition of “Lyme disease” to mean just arthritis in a knee) Wormser reported that Steeres blotting method was only detecting 15% of cases.
“Overall, 51 of 59 (86%) convalescent phase serum specimens were reactive by IB [Dearborn criteria Immunoblot-KMD], 35 of which were interpreted as positive; 26 based on IgM criteria, 8 based on both IgM and IgG, and 1 based on IgG criteria…”
Serodiagnosis in Early Lyme disease
Here are some links with some detailed chronology of the crime:
The Conspirators, they own the patents and changed the testing
Cryme time line
As anyone can see, this man belongs in prison, not in the Working Group.