Will Canada make a major announcement about Chronic Fatigue Syndrome and Ampligen today?

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You are cordially invited to an important announcement regarding myalgic encephalomyelitis in the presence of the Honourable Ginette Petitpas Taylor, Minister of Health, and Ms. Rachel Bendayan, Member of Parliament for Outremont.


 Date :   Thursday, August 22, 2019
 Time :   2h00 p.m.
Place :  Amphitheater 125, first floor, block 11 
CHU Sainte-Justine
3175, chemin de la CĆ“te-Sainte-Catherine
Montreal (Quebec) H3T 1C5

The event will be available in live streaming at the following link : https://livestream.com/CHUSteJustine/events/8789125





There is some buzz about an Ampligen activist named Scott Simpson being flown in for the Canadian CFS press conference. 



Scott Simpson was mentioned in this 2018 press release:

Scott Simpson, an ME patient and advocate with Millions Missing Canada said, "With over 580,000 Canadians diagnosed with ME, and experiencing the highest rates of unmet health care needs according to Health Canada, access to Ampligen is our greatest hope for treatment. For over 3 decades there have been millions of dollars missing from ME research and treatment in Canada, now Canadians living with ME may have a treatment option through the Special Access Program and we are keen to collaborate with Hemispherx and myTomorrows to make that opportunity become a reality. We may get our health, and lives, back."


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-
Source:  https://journals.sagepub.com/doi/10.1177/2058738418812342 A compromised paraventricular nucleus within a dysfunctional hypothalamus: A novel neuroinflammatory paradigm for ME/CFS Original Abstract A neuroinflammatory paradigm is presented to help explain the pathophysiology of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). The hypothalamic paraventricular nucleus (PVN) is responsible for absorbing and processing multiple, incoming and convergent ‘stress’ signals, and if this cluster of neurons were affected (by neuroinflammation), the ongoing hypersensitivity of ME/CFS patients to a wide range of ‘stressors’ could be explained. Neuroinflammation that was chronic and fluctuating, as ‘inflammatory-marker’ studies support, could reflect a dynamic change in the hypothalamic PVN’s threshold for managing incoming ‘stress’ signals. This may not only be a mechanism underpinning the characteristic feature of ME/CFS, post-exertional malaise, and its associated ...
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This is what oral Kaposi's Sarcoma looks like. Source:  https://doctorspiller.com/kaposis-sarcoma/ Compare it to these crimson crescent lesions in the mouths of Chronic Fatigue Syndrome patients. "Burke A. Cunha, MD, discovered what he called crimson crescents in the mouths of 80% of his CFS patients. After the word got out, Cunha received calls from other parts of the country. Physicians began telling him that they also were finding the crimson crescents in their patients once they looked for them." https://www.prohealth.com/library/crimson-crescents-facilitate-chronic-fatigue-syndrome-cfs-diagnosis-11266 Chronic Fatigue Syndrome patients may have undiagnosed internal Kaposi's Sarcoma. Susan Levin found HHV-8, the Kaposi's Sarcoma virus, in half of CFS patients she looked at. Prevalence in the Cerebrospinal Fluid of the Following Infectious Agents in a Cohort of 12 CFS Subjects Susan Levine Published online: 04 Dec 2011 ABSTR...
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  HHV-6A infection induces expression of HERV-K18-encoded superantigen Albert K. Taia, Janos Lukab, Dharam Ablashi, Brigitte T. Huber published online 08 June 2009. Abstract Background The human endogenous retrovirus K-18 (HERV-K18) encodes a superantigen that causes deregulation of the immune system. This provirus is transcriptionally silent, but can be induced by Epstein–Barr virus (EBV) infection and IFN-Ī± treatment. Objectives Since the herpesvirus EBV induces HERV-K18 expression in human B cells, it was of interest to determine if other herpesviruses would have similar HERV-K18 transactivation properties. Human herpesvirus (HHV)-6A, a neurotropic virus associated with multiple sclerosis, was a logical candidate for these studies. Study design HSB2 cells (HHV-6-negative control), HSB2-ML cells (containing latent HHV-6A genome) and HSB2/HHV-6A cells (HSB-2 cells productively infected with HHV-6A) were compared for their level of HERV-K18 transcription, using quantitative RT...
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