COVID-19’s Biological Politics

2005 study

But this is not Fau Chi’s research team, it’s the CDC.
 
At the risk of adding a link pertaining to MERS that I’ve shared on another thread but in case reading prisoners haven’t reviewed it:

Was NIH-funded work on MERS virus in China too risky? Science examines the controversy”

This is a fine addition to the archive, but Daszak collected another virus in 2011 that went to Baric’s lab for manipulation. Futhermore, it’s kind of dumb that Eco Health and NIH are playing these games of viral intrigue, when SARS-CoV-2s’ closest relative, RaTG13, only basically differs at the furin cleavage site, which SARS-CoV-2 has though RaTG13 does not. So where the action really is, is to review the story of the Tongguan miners’ cases in Kunming Hospital, because the Wuhan lab was called out at that time (2012) for having published a study stating that these SARS-CoV-like viruses could not jump from bat to human. This call-out came from the Kunming Institute of Zoology. So whatever killed the miners, RaTG13 still came from the same place.
 
This is a fine addition to the archive, but Daszak collected another virus in 2011 that went to Baric’s lab for manipulation. Futhermore, it’s kind of dumb that Eco Health and NIH are playing these games of viral intrigue, when SARS-CoV-2s’ closest relative, RaTG13, only basically differs at the furin cleavage site, which SARS-CoV-2 has though RaTG13 does not. So where the action really is, is to review the story of the Tongguan miners’ cases in Kunming Hospital, because the Wuhan lab was called out at that time (2012) for having published a study stating that these SARS-CoV-like viruses could not jump from bat to human. This call-out came from the Kunming Institute of Zoology. So whatever killed the miners, RaTG13 still came from the same place.
We’ll post the sequence of this controversial HKU4 as well as the RaTG13 sequence for comparison. The reader can go to each location when it comes up, for example in the Omicron mutation N969K, or when they come across MERS sequences, etc.

The best origin study for SARS-CoV-2’s closest relative came from India:

HKU4 Spike

RaTG13 Spike
 
The first thing we see with HKU4 when comparing Omicron’s 3-aa insertion: 214EPE, is that RaTG13 and SARS-CoV-2 is R214, while HKU4 is like Omicron, E214(glutamic acid, 4 hydrogens, 2 nitrogens). Since yak and porcine PHEV are very similar sequences, yak is 214Q (glutamine, 4 hydrogens, 1 nitrogen), PHEV is also Q.
 
For example, Omicron has N501Y mutation as does Alpha variant. Delta does not. HKU4 is Y501, and MERS is N501, which is a clue to manipulation potential at that position.
 
The following is a Scottish example of confusion between a variant and the mutations that comprise a variant, the report never thinks to ask if Omicron is (the[italics]) variant to get infected with for the best naturally-derived immunity:

Scotland: Omicron Closes School
‘....Renfrewshire Council said: “This is due to COVID-19 cases linked to the school confirmed as being, or with the potential to be, the new Omicron variant.” ‘

Old Spike Mutations That Comprise Omicron
T95I
del 69-70
D614G
K417N
N501Y
 
One news source, al-Arabiya, says that the PCR machine at Steve Biko Academic and Tshwane hospitals cannot test for Omicron S gene.

This source reports children:
 
This Omicron video includes Fau Chi’s discourse. Senator Ron Johnson calls Fau out at timepoint 6:00 and we have text to support Johnson’s claims. Fau asks “What is it going to be as it competes with Delta?“

@3:15 Boosters are going to be critical.”

@4:20 If you get boosted....maybe a considerable degree of protection

But the boosters themselves may cause mutations, just as vaccination may have caused Omicron mutations in South Africa.
 
In the first place, Fau Chi is lying, and knows that Johnson nails him on the hype for HIV. In addition, viral loads in nasal passage, mouths, noses and throats are not affected by boosters or vaccination, And remain the same in both vaxxed and unvaxxed, unless they come from within the host to rest on those surfaces, at which time they may recombine and be transmitted to another host.

’Viral Load Does Not Necessarily Correlate to Illness.
Yet another acute embarrassment to Gallo’s hypothesis is the problem of viral load. With most bacteriological and viral illnesses, increased viral load correlates with the progression of the disease and declines the patient’s health. If HIV is the sole cause of AIDS, titers should be able to track an increase in viral loads as physical deterioration progresses. Traditional viruses such as herpes, influenza, smallpox, etc., only cause disease at very high titer — thousands or millions of infectious units per cubic m illimeter of infected tissue.

In contrast, HIV has proven barely to be found in AIDS patients even in the final throes of illness. HIV can be detected, but only with difficulty, because even the sickest AIDS patients simply don’t have much virus to be found. And even m ore baffling, neither Dr. Fauci nor Gallo has ever credibly explained the fact that viral load from HIV is always at its greatest in the days immediately following infection. Logically, it would be during this period that the virus is most likely to be causing devastating illness. And yet, the onset of AIDS symptoms almost always arrive decades later (an average twenty years following exposure_ — when viral loads are at their lowest.

In 2006, a study published in the Journal of the American Medical Association (JAMA) once again shook the foundation of the past decade of AIDS science to its core and incited apoplexy among many HIV/AIDS adocates. A US nationwide team of orthodox, mainstream AIDS researchers led by doctors Benigno Rodriguez and Michael Lederman of Case Western Reserve University in Cleveland Strongly challenged the claimed legitimacy of viral load testing — the standard method since 1996 for assessing patient health, predicting disease progression, and winning grant approval for new AIDS drugs. Their study of 2,800 positively tested people concluded, in over 90 percent of cases, viral load measures failed to predict or explain immune status.’
(Kennedy, The Real Anthony Fauci, pp. 198-9)
 
Dr. Campbell’s Omicron video shows charts of various countries and one can see that Delta is leveling off.

 
After having killed 5.2 million people, SARS-CoV-2 seems to be weakening. This video extrapolates into 2022:
 
The absurdity of the new normal: accepting that the reservoir of a virus that has killed 5.2 million remains unknown.
 
Here we’ll link Omicron insertion 214EPE to the AstraZeneca COVID-19 vaccine. This vaccine is based on a chimpanzee adenovirus obtained from The Gambia. Because the information is esoteric, there are no statistics separating those Omicron patients who were vaxxed from those infections in the unvaxxed, or if vaxxed, which type of vaccine was used.

SARS-CoV-2 Spike Positions 210-220, followed by its closest relative, RaTG13 from the Mojiang copper mine. Position 214 is not capitalized.
INLVrDLPQGF
INLVrDLPPGF

DARS-CoV-2 uses receptors ACE2 and TMPRSS. We next link TMPRSS2 to COVID autopsies via Sjogren’s and Hashimoto’s:

COVID Autopsies / Hashimoto’s / Sjogren’s, post #44
’....Sjogren’s syndrome, an inflammation of the salivary and lacrimal glands.’

In post #45 of the above thread, is linked SARS-CoV-2 receptor TMPRSS to V-ets avian erythroblastosis virus.

In post #48 of that thread, Erythroblastosis virus E26 oncogene (cancer gene) is linked to Sjogren’s connecting back to the COVID autopsies. Avian Erythroblastosis virus Strain E4 links to Hashimoto’s thyroiditis revealed at COVID autopsy:

To further explain how the E26 oncogene fist into the scheme, GAG protein from Strain ES4:
’Acts as a thyroid hormone receptor antagonist. The v-Erb oncogene cooperates with v-ErbB and other primary sarcoma-inducing oncogenes in transformation of erythroblasts. THRA, the cellular counterpart of of v-ErbA, is a thyroid hormone receptor alpha....Recruits proteins of the host ESCRT machinery (Endosomal Sorting Complex Required for Transport) or ESCRT-associated proteins.’

Next we link human adenovirus pre-protein 6 to the L domains before comparing AstraZeneca’s chimp-based vaccine virus:

Like the SARS-CoV-2 spike protein, this adenovirus protein lyses the endosome. SARS-CoV-2 spike mutation D614G links precisely to a vesicular virus, VSV (vesicular stomatitis virus):

Human Mastadenovirus Pre-Protein VI / L3 Gene
‘....Endosome lysis protein; late budding domains (L domains) are short sequence motifs essential for viral particle release, interacting with proteins of the multivesicular body (MVB) pathway. Most of these proteins are class E vacuolar protein-sorting factors belonging to ESCRT-1, ESCRT-2, or ESCRT-3 complexes.
....
Mincor capsid protein 6 contains one L domain: a PPXY motif which binds to the WW domains of HECT (homologous to E-6-AP C-terminus) E3 ubiquitin ligases, like NEDD4. In adenoviruses, this motif seems to play a role in microtubule-dependent intracellular trafficking toward the nucleus during virus entry into the host cell and in suppression of DAXX-mediated repression of the immediate early E1.’

The PPXY motif means that X can be any amino acid. This motif occurs between positions 150 and 156 of AstraZeneca’s chimpanzee Y25 strain Pre-Protein 6:

150-156
EPPPYEE

This is an intriguing sequence considering the Omicron insertion 214 EPE, which may point to the second vaccine clue expressed by Omicron, the first being N969K in the heptad region 1 of the SARS-CoV-2 spike.


AstraZeneca’s chimp virus from
m The Gambia is Strain Y25
 
The argument is that more have been hospitalized since its worldwide spread and Omicron's South Africa beginning, where many had already had coronavirus infections, which points to a head-start for natural immunity.

Germany: Omicron Impossible to Stop Now
 
Immediate prophylaxis, a la Uttar Pradesh with HCQ and ivermectin, will stop Omicron in the U.S. However, American prisoners do not have access to this prophylaxis unaccompanied by stigmatization. Nor do they have access to the actual, real, entire SARS-COV-2 virus vaccine, India's Covaxin.
 

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