Blowing the Whistle at the FDA, Jan 2001, exposing Dearborn and how OspA causes immunosuppression rather than, "was a vaccine."

15 Oct 2016



Immunosuppression-its-a-thing/ - blog (There is no NIIID, hello.  Why;  Autism vaccines.)

Key Scientific Concepts - Exported fungal antigens inhibit apoptosis

Lyme Cryme: How it all Went Down

Crymes on Vimeo

DOJ protest group


Occam's Razor


IDSA says pedi-vaccines = too many, not vetted and given too young.

CDC knew OspA caused disease


BlumenthalAntiTrust Lawsuit

Exosomes, Blebs



Dattwyler, 1988
Golightly, 1988
Dressler, 1994
BarbourFish, 1993
Dearborn, 1994

Pathogenic Fungi

Predicting all of GW Bush's warcrimes, Oct 2000



Steere's "Seronegative Lyme" Hysteria about OspA-induced Antibody Inhibition
Read about it also in the 1998 FDA LYMErix meeting transcript:

; Steere using Dattwyler and Volkman's Seronegative Lyme Assay (developed because Dattwyler knew fungal antigens produced immunosuppression) to evaluate "Chronic Neurologic Lyme" cases:

See Also, CRYMEDISEASE_CHP3_B.htm  where we show Steere in 1991 actually used this seronegative Lyme assay on his own lab
workers, 101016.htm (  where we see Steere knowingly falsely advising the Academy
of Insurance Medicine a year later (1992), and the Plum Island Chapter of Cryme Disease where Justin Radolf demonstrates in 2001
that OspA vaccination (or autovaccination via blebbing), results in inhibition of antibody production via downregulation of HLA.

N  1988 Dec 1;319(22):1441-6.

Seronegative Lyme disease. Dissociation of specific T- and B-lymphocyte responses to Borrelia burgdorferi.


Department of Medicine, State University of New York, School of Medicine, Stony Brook 11794-8161.


The diagnosis of Lyme disease often depends on the measurement of serum antibodies to Borrelia burgdorferi, the spirochete that causes this disorder. Although prompt treatment with antibiotics may abrogate the antibody response to the infection, symptoms persist in some patients. We studied 17 patients who had presented with acute Lyme disease and received prompt treatment with oral antibiotics, but in whom chronic Lyme disease subsequently developed. Although these patients had clinically active disease, none had diagnostic levels of antibodies to B. burgdorferi on either a standard enzyme-linked immunosorbent assay or immunofluorescence assay. On Western blot analysis, the level of immunoglobulin reactivity against B. burgdorferi in serum from these patients was no greater than that in serum from normal controls. The patients had a vigorous T-cell proliferative response to whole B. burgdorferi, with a mean ( +/- SEM) stimulation index of 17.8 +/- 3.3, similar to that (15.8 +/- 3.2) in 18 patients with chronic Lyme disease who had detectable antibodies. The T-cell response of both groups was greater than that of a control group of healthy subjects (3.1 +/- 0.5; P less than 0.001). We conclude that the presence of chronic Lyme disease cannot be excluded by the absence of antibodies against B. burgdorferi and that a specific T-cell blastogenic response to B. burgdorferi is evidence of infection in seronegative patients with clinical indications of chronic Lyme disease.

Comment in