Using LYMErix to tolerize against Bubonic Plague … or “Prevent the CDC, they’re dangerously stupid.”

[ The Dattwyler OspA-is-Pam3Cys patent is actually against inhalation vaccine against Inhalation Bubonic Plague.
IF you are the kind of person who wants a simple one-liner, single model, single, simple general idea to explain something, this would be it (Dattwyler and Fauci, below). OspA is a known immune-suppressor, not a “vaccine.”
We are not about to prove that OspA is a triacyl lipoprotein also called a basic Pam3Cys molecule type, is fungal, is a more serious endotoxin than LPS, a TLR2/TLR1 agonist, and that other spirochetal lipoproteins are triacylated, if not Pam3Cys exactly. We can assume anyone knows how to use the National Library of Medicine or else the United States and European patent databases or even just pull the one arm of one-armed information bandit named Google and discover that, for instance, State University of New York, Stony Brook’s, Raymond Dattwyler has a patent for an inhalation form of OspA.
It, the OspA in Dattwyler’s OspA patent, is intended to attenuate (lessen, or dampen) any suffocating inflammatory response people might suffer from the likes of the dual infections of, for example, influenza and pneumonia, such as what happened in the 1918 Spanish Flu epidemic [FAUCI]. During that pandemic, the healthy people succumbed to the secondary pneumonia. That is, the strong, mucus-y inflammatory response is what killed 20+ million people back then. They choked to death. (One infection invites another, this is well-known).
Let’s just go ahead and have a look at what Raymond Dattwyler says about OspA as Pam3Cys and how inhaling a fungal antigen like this, OspA or Pam3Cys or a triacyl lipoprotein might tolerize you against the deadly pneumonia part of Pandemic Flu-monia:
“A lipidation/processing reaction has been described for the intact OspA gene of B. burgdorferi. The primary translation product of the full-length B. burgdorferi OspA gene contains a hydrophobic N-terminal sequence, of 16 amino acids, which is a substrate for the attachment of a diacyl glyceryl to the sulflhydryl side chain of the adjacent cysteine (Cys) residue (at position 17). Following this attachment, cleavage by signal peptidase II and the attachment of a third fatty acid to the N-terminus occurs. The completed lipid moiety, a tripalmitoyl-S-glycerylcysteine modification, is termed Pam3Cys (or is sometimes referred to herein as Pam(3)Cys or Pam3Cys). It has been suggested that the lipid modification allows membrane localization of proteins, with polypeptide portions exposed as immune targets. In addition to serving as targets for the immune response, Pam3Cys-modified proteins, such as OspA, have been reported to act as potent inflammatory stimulants though the toll-like 2 receptor mechanism (TLR2).
NIAID’s Chief Anthony Fauci on the ‘monia part of 1918 Spanish Flumonia® being what causes people to choke to death — it was inflammatory response in the lungs to the fungal-ish pneumonia:
J Infect Dis. 2008 Oct 1;198(7):962-70. doi: 10.1086/591708.
Predominant role of bacterial pneumonia as a cause of death in pandemic influenza: implications for pandemicinfluenza preparedness.
Morens DM1, Taubenberger JK, Fauci AS.
Author information
Despite the availability of published data on 4 pandemics that have occurred over the past 120 years, there is little modern information on the causes of death associated with influenza pandemics.
We examined relevant information from the most recent influenza pandemic that occurred during the era prior to the use of antibiotics, the 1918-1919 “Spanish flu” pandemic. We examined lung tissue sections obtained during 58 autopsies and reviewed pathologic and bacteriologic data from 109 published autopsy series that described 8398 individual autopsy investigations.
The postmortem samples we examined from people who died of influenza during 1918-1919 uniformly exhibited severe changes indicative of bacterial pneumonia. Bacteriologic and histopathologic results from published autopsy series clearly and consistently implicated secondary bacterial pneumonia caused by common upper respiratory-tract bacteria in most influenza fatalities.
The majority of deaths in the 1918-1919 influenza pandemic likely resulted directly from secondary bacterial pneumonia caused by common upper respiratory-tract bacteria. Less substantial data from the subsequent 1957 and 1968 pandemics are consistent with these findings. If severe pandemic influenza is largely a problem of viral-bacterial copathogenesis, pandemic planning needs to go beyond addressing the viral cause alone (e.g., influenza vaccines and antiviral drugs). Prevention, diagnosis, prophylaxis, and treatment of secondary bacterial pneumonia, as well as stockpiling of antibiotics and bacterial vaccines, should also be high priorities for pandemic planning.
So, if OspA was obviously something that causes too-much inflammation-and-then-immunosuppression (endotoxin tolerance), it could not have been a vaccine. And if OspA was not a vaccine, then certain people not only lied it onto the market, they falsified the Dearborn case definition to leave out the 85% of us who do not have a genetic background for a tendency to have Rheumatoid Arthritis (HLAs).
So, IF you are the kind of person who wants a simple one-liner, single model, single, general idea to explain something, this would be it. OspA is a known immune-suppressor, not a “vaccine.” It does the OPPOSITE of what vaccines are intended to do, which is produce antibodies. It is a more severe endotoxin than LPS.
“TLR2 mediates inflammatory responses to a wide variety of lipidated microbial components, including bacterial lipoproteins, atypical lipopolysaccharides, and lipomannans (26–28). Among these microbial agonists, bacterial lipoproteins are by far the most potent (26, 29–31).”
See the rest of the videos here: Crymes on Vimeo

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