Welcome to ActionLyme - the Lyme Cryme Whistleblower's Website

1-Yale Defrauds Govt Steere falsifies case definition, 1992 USDOJ RICO Complaint 30 reports; Sepsis, Autism UN Complaint (2003) Bioweapons Attributes
2-Who owns the patents? CDC's Patents w/ GSK, 1992 Blumenthal (AntiTrust) AIDS-like EBV-Borreliosis, 101016 Antics Crazy Eddy & Durl Lyme as a bioweapon?
3-Who identified the biomarkers? Great Imitator/IDSA "Reviews", 1989 False Claims Act case, ref'd OspA / Pam3Cys Tolerance Munchausen's Libel Army says Bioweapon
4-NIH's Post Sepsis Syndrome Congenital Lyme by Yale Cold Spring Harbor, neuroLyme Failed Other Fungal Vax Sweeg's Munchausen's Russians@NYMC (HLAs)
5-IDSA's DNA Shell Game Halperin: Lyme & ALS Relapsing Fever, permanent, IDSA too PubMed: OspA >> EBV ALDF.com files Plum Island Evidence
6-Commonalities (CFIDS & Autism) Steere: Lyme >> Lupus Dattwyler: Seroneg Lyme LYMErix causes neurologic Fish @ Internat.Spy Firm EXOSOMES/BLEBS
7-UConn Assaults Czech kids Klempner & "Guidelines" Steere: Seronegative Lyme NIH:  CLD is active herpes Durland Fish's "Attack" Lyme Mafia Alpert
8-Wessely & Somatoformers McSweegan attacks Navy, 1986 .CORIXARICO

ME/CFS is active herpes

Lyme Mafia Sepkowitz

11/28/2015 12:53:43


Navigation, File Lists:
criminal charges, video PPT series, chronology, ICD-10 codes to use.

THE LIST of real scientists - none in IDSA or ILADS.

2 things 2 know
SASH sites:
Bad Lyme Attitude


"Spirochetes May Love the Brain to Death"

Benach/IDSA, brain damage in Lyme, 1992 (scanned)

Exosomes, Vesicles, Blebs

SASH vaccines paper (Common Mechanisms)

Spirochetal Dementia


CDC/Yale/IDSA: "LYMErix causes  same multisystem disease" as 'Chronic Lyme'"  OspA is a fungal toxin causing immunosuppression



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 (
http://www.ncbi.nlm.nih.gov/pubmed/1883122)  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.

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