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Influenza Caused Epidemic Encephalitis (Encephalitis Lethargica): The Circumstantial Evidence and a Challenge to the Nonbelievers
C P Maurizi. Med Hypotheses. May 2010
Surprisingly two different viruses were involved with the great pandemic. A single amino acid difference in the hemagglutinin of the two viruses changed the preferred receptor of the virus in the host cell. One virus has qualities that suggest that it is neurovirulent. Circumstantial evidence suggests that the cause of death in some influenza patients was neurogenic congestive heart failure with pulmonary edema.
Geneticist Rotem Sorek could see that his bacteria were sick — so far, so good. He had deliberately infected them with a virus to test whether each ailing microbe soldiered on alone or communicated with its allies to fight the attack.
But when he and his team at the Weizmann Institute of Science in Rehovot, Israel, looked into the contents of their flasks, they saw something completely unexpected: the bacteria were silent, and it was the viruses that were chattering away, passing notes to each other in a molecular language only they could understand.
They were deciding together when to lie low in the host cell and when to replicate and burst out, in search of new victims.
It was an accidental discovery that would fundamentally change scientists’ understanding of how viruses behave.
originally posted by: Oleandra88
a reply to: one4all
So what you are saying, since we are on a conspiracy site is that
The elite released the virus as a gift to us because we will learn how to cure cancer from it while thinning out the sick and weak.
But then -plot twist- you just get the vaccination that comes along with the mini chip tag. You know what a TENS unit is? It is formidable for BDSM sessions. They can really hurt. Imagine you have one in your bloodstream.
They turned the secret advice to put tinfoil around the head into a deadly weapon.
it is all sarcasm and garbage I need to distract myself.
So far, most cases on the U.S. West Coast are linked to a strain first identified in Washington state. It may have come from a man who had been in Wuhan, China, the virus’ epicenter, and returned home on Jan. 15. It is only three mutations away from the original Wuhan strain, according to work done early in the outbreak by Trevor Bedford, a computational biologist at Fred Hutch, a medical research center in Seattle.
On the East Coast there are several strains, including the one from Washington and others that appear to have made their way from China to Europe and then to New York and beyond, Chiu said.
The COVID-19 virus does not mutate very fast. It does so eight to 10 times more slowly than the influenza virus, said Anderson, making its evolution rate similar to other coronaviruses such as Severe Acute Respiratory Syndrome (SARS) and Middle East Respiratory Syndrome (MERS)
While the maps are fun, they can also be “a little dangerous” said Andersen. The trees showing the evolution of the virus are complex and it’s difficult even for experts to draw conclusions from them.
“Remember, we’re seeing a very small glimpse into the much larger pandemic. We have half a million described cases right now but maybe 1,000 genomes sequenced. So there are a lot of lineages we’re missing,” he said
Coronavirus strains are maintained in quasi-species pools circulating in bat populations. (a,b) Traditional SARS-CoV emergence theories posit that host-range mutants (red circle) represent random and rare occurrences that permit infection of alternative hosts.
The secondary-host paradigm (a) argues that a nonhuman host is infected by a bat progenitor virus and, through adaptation, facilitates transmission to humans; subsequent replication in humans leads to the epidemic viral strain.
The direct paradigm (b) suggests that transmission occurs between bats and humans without the requirement of an intermediate host; selection then occurs in the human population with closely related viruses replicating in a secondary host, permitting continued viral persistence and adaptation in both.
(c) The data from chimeric SARS-like viruses argue that the quasi-species pools maintain multiple viruses capable of infecting human cells without the need for mutations (red circles). Although adaptations in secondary or human hosts may be required for epidemic emergence, if SHC014 spike–containing viruses recombined with virulent CoV backbones (circles with green outlines), then epidemic disease may be the result in humans. Existing data support elements of all three paradigms.
On the origin and continuing evolution of SARS-CoV-2
The SARS-CoV-2 epidemic started in late December 2019 in Wuhan, China, and has since
impacted a large portion of China and raised major global concern. Herein, we investigated
the extent of molecular divergence between SARS-CoV-2 and other related coronaviruses.
Although we found only 4% variability in genomic nucleotides between SARS-CoV-2 and a bat SARS-related coronavirus (SARSr-CoV; RaTG13), the difference at neutral sites was 17%, suggesting the divergence between the two viruses is much larger than previously estimated.
Our results suggest that the development of new variations in functional sites in the receptor-binding domain (RBD) of the spike seen in SARS-CoV-2 and viruses from pangolin SARSr-CoVs are likely caused by mutations and natural selection besides recombination.
Population genetic analyses of 103 SARS-CoV-2 genomes indicated that these viruses evolved into two major types (designated L and S), that are well defined by two different SNPs that show nearly complete linkage across the viral strains sequenced to date.
Although the L type (~70%) is more prevalent than the S type (~30%), the S type was found to be the ancestral version. Whereas the L type was more prevalent in the early stages of the outbreak in Wuhan, the frequency of the L type decreased after early January 2020.
Human intervention may have placed more severe selective pressure on the L type, which might be
more aggressive and spread more quickly. On the other hand, the S type, which is evolutionarily older and less aggressive, might have increased in relative frequency due to relatively weaker selective pressure.
These findings strongly support an urgent need for
further immediate, comprehensive studies that combine genomic data, epidemiological data,
and chart records of the clinical symptoms of patients with coronavirus disease 2019
Keywords: SARS-CoV-2, virus, molecular evolution, population genetics
originally posted by: HelloboysImbackguy
a reply to: one4all
Thats really interesting. I was going to let this thread die but your thought process and the other comment about anamorphic Bacterias....and the odd outer fat layer.
I dont know enough about this to even talk coherently about it without losing my own thoughts.
Im going to do some homework and think about it.
Im wondering if somehow this thing is the using natural bacteria in our digestive system located near the respiratory trach opening and it just spreads down..There are some unexplained digestive issues this thing causes......its maybe using the bacteria to form the outer fat layer, or harvesting resources from the bacteria to make the fat layer while in new cells it is infecting.
Maybe its symptoms differ according to where it first sets roots....since it is using different tissues to make similar structures...
Lots of good ideas with that one. Thanks for contributing to all of you!