New myth circulating in the Lyme community: That it would be bad for the Lymish to force vaccinate the Lymish.
Recombinants would have no effect, since you have no immune system. Yet either type of live viral vaccine however upon the Lymish might force the next mutation in that disease they are trying to prevent … and possibly make it more virulent. Dont forget, how the pandemic 1918 flu worked was a bird flu and a swine flu together in the same animal, swapping DNA – since after all, dual or multiple infections suppress the immune response for both/all (keep reading since I have the proof if this in this post, below).
Everyone should be laughing at the idea that we have something to fear from vaccines. It is everyone else who should be terrified of the Lymish being forced to get extra vaccines, especially live viral ones. We have no immune system. A recombination paradise. Everything mixes with everything else 😀
Look at two sources here:
“The major troop staging and hospital camp in Étaples, France, was identified by researchers as being at the center of the Spanish flu. The research was published in 1999 by a British team, led by virologist John Oxford.[20] In late 1917, military pathologists reported the onset of a new disease with high mortality that they later recognized as the flu. The overcrowded camp and hospital was an ideal site for the spreading of a respiratory virus. The hospital treated thousands of victims of chemical attacks, and other casualties of war. 100,000 soldiers were in transit through the camp every day. It also was home to a live piggery, and poultry was regularly brought in for food supplies from surrounding villages. ***Oxford and his team postulated that a significant precursor virus, harbored in birds, mutated and then migrated to pigs kept near the front.[21][22]” ****
https://en.wikipedia.org/wiki/Spanish_flu
And the murdered scientist (really, this time) Don C. WIley:
“In contrast, the H9 swine and H3 human virus HAs recognize the cis conformation of the α2,6 and α2,3 glycosidic linkage, where the linkage carbon atoms of Gal-2 C6 in LSTc and Gal-2 C3 in LSTa and the Gal-2 ring of LSTa make nonpolar contacts with Leu-226 (Fig. (Fig.22 e and f and figure 2 in ref. 19) and the glycosidic oxygen points toward solution. α2,6 apparently is favored by the H9 swine HA (Fig. (Fig.33f) because only sialic acid and Gal-2 of the oligosaccharide are detected interacting with the HA in the α2,3 pentasaccharide sialoside complex (Fig. (Fig.33e). The width of avian virus-binding sites is narrower than the swine and human HA sites, which appears to optimize contacts with the preferred sialoside linkages. The H9 swine HA with Leu-226/Gly-228 may represent an evolutionary intermediate (33), with a binding site not yet as optimal for human cells as the human 1968 H3 site (Fig. (Fig.44).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC58807/
Cross pollination (lol) and “antibody selection pressure,” anyone? Here is Lymish Pandemic Soup:
“Because the IAV genome consists of eight discrete RNA segments, co-infection of one host cell with two different IAVs can result in progeny viruses containing gene segments of both parental viruses. When this process of genetic reassortment involves the gene segments encoding the HA and/or NA genes it has been termed antigenic shift. There are theoretically 256 (28) possible combinations of the eight gene segments from reassortment between two parental viruses. Reassortment has been shown to be both common and important in IAV evolution (Dugan et al., 2008; Holmes et al., 2005) and host switch events (Garten et al., 2009; Scholtissek et al., 1978). Homologous recombination is not common in negative sense RNA viruses like IAV (Boni et al., 2008), but recombination by template switching has been described and has played a role in changing the virulence or fitness of some IAVs (Wright et al., 2007).”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2892379/
It wont affect us; we dont have an immune system, and the way the flu works is to cause IMMUNOSUPPRESSION which then invites in the mycobacteria (pneumonia) and people die from a strong immune response to the … wait for it, … secondary opportunistics like pneumonia. Most of us probably already have tuberculosis or pneumonia. We are just not sneezing it all over everyone else because… we have no immune system.
We Lymish dont have to worry. We wont die of secondary flu-monia. We will instead probably be helping it – or anything else – to mutate into a more virulent strain….
I really wish the non-scientists who put out all this nonsense would shut the hell up. Stop running your mouth unless you really know what you are talking about. The model we have presented does not change. See the charge sheets on truthcures.org or actionlyme.org.
Here i HAVE SHOWN YOU AGAIN… THE SAME MODEL. . Flu….monia. See all of that wikipedia page…
co-infection of one host cell with two different IAVs can result in progeny viruses containing gene segments of both parental viruses.
^^^ Dont forget THAT ^^^. That is how we Lymish are pandemic disease factories. One of the reasons they (CDC) dont want to give us antibiotics is because they claim we will be developing resistant strains of bacteria. They know. 😉
They KNOW we are chock full of infectious diseases. 😉
Lym-phoid Marys, Lymish Flu Pandemic of 2019… etc
Dont worry. Everyone else needs to worry. This will be the Karma we all have been waiting for… 😉
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Cryme Disease - Unscrambling the CDC's DNA Patent Profiteering Bullshit 