Ben Luft (SUNY-SB), at the 1998 FDA committee meeting on LYMErix (These references are all in the charge sheets)
1) Ben Luft said it at the 1998 FDA meeting:
BEN LUFT: “The point that I wanted to make in regard to the study is that there is very heavy dependence on serologic confirmation. And when we start thinking about the adverse events, *** it was stated originally when we got the overview of the disease that the disease is really quite protean. And actually the adverse events are very similar to what the disease manifestations are.****
Dave Persing in his patent for a method he worked out with Yale’s Robert Schoen as the RICO within the RICO for the 3 labs that wanted to capture all the post-LYMErix testing in north America:
Method for detecting B. burgdorferi infection
“…Additional uncertainty may arise if the vaccines are not completely protective; vaccinated patients with multi-system complaints characteristic of later presentations of Lyme disease may be difficult to distinguish from patients with vaccine failure.”
Ray Dattwyler (SUNY-SB) talking about how Borrelial hydrophobic lipid antigens (supernatant) are responsible for the diminution of NK cell activity in 1988:
Ann N Y Acad Sci. 1988;539:103-11.
Modulation of natural killer cell activity by Borrelia burgdorferi.
Golightly M1, Thomas J, Volkman D, Dattwyler R.
“Effect of B burgdorferi Culture on Normal PBL
”…when lymphocytes are cultured in the presence of growing Bb there is a marked inhibition ( p < .0005 ) of NK activity on days 3, 5, and 7 when compared to lymphocytes cultured in BSKII media in the absence of spirochetes. This effect is not due to a selective depletion or toxicity to endogenous NK since viability studies and monoclonal antibodies demonstrate no significant changes after culture with the organism.
“The inhibition is directly attributable to the organism or its supernatants (data not shown).”
Donald Marks, an OspA vaccine trial administrator said to the FDA IN PERSON (and also published about this):
“Today I am here as a consultant of the Lyme Disease Association, which has asked me to review a series of adverse events associated with Lymerix: These include athralgias and arthritis as well as complicated neurological problems. They include adverse events that are long-lasting.
Dr. Marks proceeded to present a series of slides. We reproduce them here, with explanation and some editing, where needed, for clarity and brevity in the current context.
WHY MORE ADVERSE EVENTS WERE SEEN AFTER THE VACCINE REACHED THE MARKET:
- People receiving Lymerix after product launch were at greater risk for adverse events because they lived in Lyme-endemic areas.
- Many of these people may have had prior exposure and clinical or subclinical infection. In these cases, Lymerix could be triggering or reactivating the damage caused by old and presumably cured Lyme disease.
- Pattern of symptoms experienced after Lymerix mimicked pattern of prior infections in many individuals. In these patients, Lymerix-related symptoms seemed to respond to antibiotics, as did the initial infection, bolstering the theory of disease reactivation.
HOW SMITHKLINE BEECHAM (GLAXO SMITHKLINE) USED CONFUSING LANGUAGE, KEEPING FDA AND PHYSICIANS IN THE DARK:
- The Company dismissed the significance of adverse events reported since marketing by stating the vaccine’s profile had not changed “except as described below…” The description referred to, rendered with numbers but given no contextual explanation, in fact implied a huge change in safety. The company’s confusing language made it sound as if the adverse events, many of them severe, had no particular significance at all.
- As proof of safety, the company inoculated arthritis-prone mice with Osp-A. But since the mice did not possess the HLA marker known to interact with Osp-A in humans, the experiment was, in fact, meaningless.
- The company has masked serious causally-related adverse events behind qualifiers, such as “…and which may have no causal relationship with the vaccine” and “…cannot be distinguished from the natural history of the underlying disease,” all the while knowing these are confusing the issues.
And Martin and Marques (say who they were):
Borrelia burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral blood monocytes but differentially regulates HLA-class II expression.
- Cellular Immunology Section, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892, USA. firstname.lastname@example.org
The spirochete Borrelia burgdorferi is the agent of Lyme disease, which causes central nervous system manifestations in up to 20% of patients. We investigated the response of human brain microglial cells, glial progenitors, neurons, astrocytes, as well as peripheral blood monocytes to stimulation with B. burgdorferi. We used oligoarrays to detect changes in the expression of genes important for shaping adaptive and innate immune responses. We found that stimulation with B. burgdorferi lysate increased the expression of Toll-like receptors (TLRs) 1 and 2 in all cell types except neurons. However, despite similarities in global gene profiles of monocytes and microglia, only microglial cells responded to the stimulation with a robust increase in HLA-DR, HLA-DQ, and also coexpressed CD11-c, a dendritic cell marker. 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.