- Messages
- 41
We are certain you’ve all seen by now the final public admissions by the Governments of Norway and the United States that ME/CFS and Chronic Lyme are really the same thing as post-sepsis syndrome, with the terrible post-sepsis immunosuppression and chronic active herpes viruses, fungal-induced immunosuppression, cross-tolerance and extreme fatigue. Also, the treatment with Rituximab and the stunning cure rate with this anti-EBV drug (CD20 is a marker for an B cells, which is where EBV hides out, which is why it is used in Leukemia and Multiple Sclerosis) confirms the mechanism of disease.
Before we even start, please read these 4 reports:
2014: Washington University, St. Louis, MO, discovers that sepsis is like Lyme, in that the survivors of it are likely to have survived via the immunosuppression (TLR2-agonist tolerance/Endotoxin tolerance), but the result is the reactivation of latent viruses:
“Dormant viruses re-emerge in patients with lingering sepsis, signaling immune suppression”http://news.wustl.edu/news/Pages/27015.aspx
FULL JOURNAL REPORT
“Reactivation of Multiple Viruses in Patients with Sepsis”http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0098819
NIH, 2014, “Surviving Sepsis: Detection and Treatment Advances” By Carolyn Beans for the National Institutes of Health | August 18, 2014 08:43am ET
http://www.livescience.com/47387-sepsis-diagnosis-treatment-research-nigms.html
Here, in the 1950s, they show you can’t inject fungi together with viruses or you get the reactivated viruses:
“IV. THE RELATIONSHIP OF EPERYTHROZOON COCCOIDES TO THE HEPATITIS VIRUS OF PRINCETON MICE”
“In Swiss mice, animals with high natural resistance to hepatitis virus, the pathogenicity of this agent was markedly enhanced by combined infection with eperythrozoa. Eperythrozoa were maintained throughout 18 successive passages in normal Princeton and Swiss weanlings with intact spleens. The combined infection of Princeton mice with eperythrozoa and the virus component of Gledhill, Dick, and Andrewes, which is nearly inactive when injected alone, resulted in acute hepatitis with fatal outcome.”
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2136329/?tool=pubmed
full article - http://www.allmov.org/usa-norway-governments-show-post-sepsis-ebv-and-rituximab/
Before we even start, please read these 4 reports:
2014: Washington University, St. Louis, MO, discovers that sepsis is like Lyme, in that the survivors of it are likely to have survived via the immunosuppression (TLR2-agonist tolerance/Endotoxin tolerance), but the result is the reactivation of latent viruses:
“Dormant viruses re-emerge in patients with lingering sepsis, signaling immune suppression”http://news.wustl.edu/news/Pages/27015.aspx
FULL JOURNAL REPORT
“Reactivation of Multiple Viruses in Patients with Sepsis”http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0098819
NIH, 2014, “Surviving Sepsis: Detection and Treatment Advances” By Carolyn Beans for the National Institutes of Health | August 18, 2014 08:43am ET
http://www.livescience.com/47387-sepsis-diagnosis-treatment-research-nigms.html
Here, in the 1950s, they show you can’t inject fungi together with viruses or you get the reactivated viruses:
“IV. THE RELATIONSHIP OF EPERYTHROZOON COCCOIDES TO THE HEPATITIS VIRUS OF PRINCETON MICE”
“In Swiss mice, animals with high natural resistance to hepatitis virus, the pathogenicity of this agent was markedly enhanced by combined infection with eperythrozoa. Eperythrozoa were maintained throughout 18 successive passages in normal Princeton and Swiss weanlings with intact spleens. The combined infection of Princeton mice with eperythrozoa and the virus component of Gledhill, Dick, and Andrewes, which is nearly inactive when injected alone, resulted in acute hepatitis with fatal outcome.”
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2136329/?tool=pubmed
full article - http://www.allmov.org/usa-norway-governments-show-post-sepsis-ebv-and-rituximab/