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COVID-19’s Biological Politics

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badger2

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A fascist USMB c.u.n.t closed the snake meat thread due to inexperience, and here we have post #440 seemingly getting us back on track after deliriously wandering off topic. Post #440 report mentions MI6’s Dearlove, whom we mentioned in post #416, with the same authors, Dagleish, Sorenson, etc. Today our trajectory focused on such things as LDLR, connecting both ebola vaccine and Alzheimer’s. The report in post #440 For CGG-CGG actually links to neurodegenerative diseases. Duh

2018 Poland: Fragile X-Associated Tremor/Ataxia Syndrome (FXTAS)

So how do these sensationalist authors explain the CGG repeats in FXTAS? The authors should be made to cough up the genome sequence of the human their COVID-19 sequence was taken from.
 
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Elderly males are implicated in CGG repeats along with toxic mRNA. Epstein:

’Fragile X syndrome is an X-linked domain disorder with reduced penetrance whose primary manifestation is moderate-to-severe mental retardation. It is most often caused by the transcriptional silencing of the FMR1 gene due to an expansion of a CGG-repeat found in the 5’ untranslated region (UTR). This allelic class, with greater than 200 CGG-repeats, is referred to as the full mutation. Normal alleles have up to 54 repeats with 30 repeats being most common....common-6-44 repeats....The second phenotype is FXTAS which is an adult-onset neurodegenerative disorder that includes progressive intention tremor, gait abnormalities, a characteristic white matter abnormality observed by MRI, and dementia. In contrast to lack of FMR1 transcription associated with FXS, the premutation-associated diseases are caused by a toxic RNA effect caused by an excessan excess of FMR1 transcription and/or repeat-containing mRNA....Drosophila. The dFXR null mutants cannot be maintained as a stock using routine technique for Drosophila. In fact, the males have a 90% reduction in fecundity that is due to an arrest in late-stage spermatid differentiation....The antagonistic connection between dFXR and (futsch[italics]) is strengthened further by the fact that the phenotype of flies with a gain of function in dFXR is similar to that of flies with a loss-of-function mutation for futsch, and the fact that loss of function mutations in futsch rescue some of the phenotypes associated with dFXR mutations.’
(Epstein CJ, Inborn Errors of Development: The Molecular Basis of Clinical Disorders of Morphogenesis, pp. 1126-31)
 
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Flapping their arrogant lips about it, they have assisted us in our knowledge of houseflies as (mechanical [italics]) vectors of COVID-19.
 
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POSPOTUS JoeXi is a catholic-CIA puppet, and does not have the intelligence to have brought up lab-leak theories. The CIA has told the media to say that it was JoeXi’s earlier intuition, which is supreme media propaganda.
 
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Post #437 mentioned VSV and lentiviral vectors, here linking them to magnetofection in an Italian report:

2016 Italy: Magnetofection / Lentiviral-Mediated Transduction
 
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The recent trajectory on this thread for Alzheimer’s and LDLR, the major receptor for VSV, now links to resurrection of an Alzheimer’s drug. We especially took notice of it due to calcium homeostasis:

7 Jun 2021 Madison.com published a report from CNN, ‘FDA Approves Aducanumab’ and it was reported in the New York Times on 5 Jun 2021.

Dec 2016 Aducanumab Restores Calcium Homeostasis

An excerpt from Future Medicine (2019) homes in on the target of aducanumab:

’....Aducanumab (BIIB037) is a recombinant human IgG1 antibody in development for treatment of prodromal Alzheimer’s disease. Aducanumab binds to soluble amyloid-beta aggregates and insoluble fibrils with > 10,000-fold selectivity over monomers. Aducanumab emerged from a large screen of B-cell clones obtained from healthy, aged donors who were cognitively normal. It recognizes N-terminal residues 3-7 of the amyloid-beta sequence....It is the first time that a lowering effect on amyloid-beta brain load by an anti-amyloid-beta therapy was coupled with a positive effect on cognition and clinical global status with dose-dependent trends.’

The N-terminal sequence of amyloid-beta is

DAEFRHDSGYEVHHQK

Thus, aducanumab recognizes the sequence EFRHD. Aspartic acid (D) begins the N-terminal sequence and ends the aducanumab sequence of recognition.

We’ve mentioned LDLR in conjunction with VSV, the basis of ebola vaccine. Here it links to Alzheimer’s:

Alzheimer’s Amyloid-Beta / LDLR

’....LDLR receptor deficiency does not alter brain amyloid-beta levels, but causes an exacerbation of apoptosis.’

We’ve mentioned Fragile X and FXTAS in the thread via Epstein, and here we link these with CGG RNA and apoptosis:

2014 FXTAS Apoptosis / CGG RNA

2005 Apoptosis CGG-Repeat RNA
 
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The CGG claim at post #440 does not show the graphics they are referring to, though they do mention furin. The claim should accompany the amino acid sequences, so that comparison and analysis can be done, especially (neighboring amino acids [italics])

We mentioned furin on the snake meat thread, post #543 one day after the following article was published, refuting pangolins due precisely to furin:

27 Feb 2020 Evolutionary History Potential Intermediate Animal Host, and Cross-Species Analysis of SARS-CoV-2
’....Interestingly, the coronavirus carried by pangolins did not have the RRAR motif (furin cleavage). Therefore, we conclude that the human SARS-CoV-2 virus, which is responsible for the recent outbreak of COVID-19, did not come directly from pangolins.’
 
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While still searching for the env retroviral integration excerpt for coronaviruses, this following report has been withdrawn:

’....the insert 1 (6 amino acid residues) and insert 2 (6 amino acid residues) in the spike glycoprotein of the 2019-nCoV are 100% identical to the residues mapped to HIV-1 gp120....it is quite unlikely for a virus to have acquired such unique insertions naturally in a short duration of time....this structural change might have also increased the range of host cells that 2019-nCoV can infect.’
 
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It was the Compton Lab that destroyed its rinderpest stock:

’....Researchers have been reluctant to destroy lab samples of deadly viruses in case they are needed to create a vaccine should the disease re-emerge. But a digital record of the virus’s genetic code means that this is no longer an issue....declared to have been eradicated in the wild in 2011.’

Compton lab is Pirbright Institute for Bill and Melinda Gates, mentioned on various USMB threads, snake meat thread on 28 Jan 2020. Here, another retroviral fact for the files:

Compton Lab, 2001: Use of Defective RNAs Containing Reporter Genes to Investigate Targeted Recombination for Avian Infectious Bronchitis Virus
‘Relative hygromycin B resistance has been used to discriminate between BCoV field isolates (Kapil, et al, 1999), but we believe that Hyg-containing recombinant IBV would have an advantage over IBV that would emerge since similar systems have been successfully used to select recombinant retroviruses (Zhang & Sapp, 1999, U. Of Kentucky, Lexington ‘Recombination between Two Identical Sequences within the Same Retroviral RNA Molecule’).’
(The Nidoviruses: Coronaviruses and Arteriviruses)
 
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Mention was made of TRIM5 in posts # 407, 408 & 432, now linking it to retroviral element integration, VSV and Drosophila gypsy, noting how vsv acts in this abstract:

HIV-1 Challenge / TRIM5alpha / Cytokine Production / VSV

Ap 2021 Seattle, Wa., Stony Brook, New York: Drosophila Gypsy / Env

A recent report from a key laboratory in Wuhan:

May 2021 Hubei Key Laboratory, Wuhan: Simeprevir / COVID-19 Salt Bridges
’....A key pair of salt bridges formed by the side chains of K537 and E619....promotes opening of the RBD. Simeprevir, imatinib and naldemedine....mutating K537Q and E619D decreased their side chain lengths and eliminated this pari of salt bridges.’

Note that the D614G mutation is in proximity, and compare mutations E484Q in the Indian and P.2 Brazil-Japan variants (P.1 Brazil-Japan is E484K).
 
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We can tentatively show a connection to a virus from Ugandan bats for comparison to hydroxychloroquine due to its mechanism of replication. We will then link it to the Nidovirus genome.
 
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As the reader may study the anatomy of the Doryrhina cyclops muzzle, note that Ft. Detrick indeed has studied Bungarus multicinctus, a suspected intermediate host of SARS-CoV-2, though has not produced any reports on the subspecies, B. m. wanghaotingi, which habitat would include the range of Mengla virus-harboring Rousettus, mentioned earlier in the thread. The differences that establish wanghaotingi as a subspecies link to anatomical differences in what we will call the “muzzle region.” Genetically, there is no apparent published genome for B. m. wanghaotingi.
 
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From the University of Wisconsin, Madison, studies revealed Doryrhina’s link to German measles:

7 Oct 2020 Newly Discovered Viruses Suggest ‘German Measles’ Jumped from Animals to Humans
’....Goldberg and his former graduate student, Andrew Bennett, discovered one of the new viruses in apparently healthy cyclops leaf-nosed-bats, netted at night in Kibale National Park in Uganda. They named it ruhugu virus, after the Ruteete region of Uganda and the local word for bat. The architecture of ruhugu’s genome is identical to that of the rubella virus, and 56% of the amino acids in its eight proteins matched those of rubella. The protein that interacts with the host’s immune cells was almost identical in both viruses. Goldberg notes, “Now we know that every disease in the letters of the MMR vaccine has a zoonotic origin.” ‘
 
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To the study that follows, a list of contributing authors:

1. Department of Pathobiological Sciences, University of Wisconsin-Madison

2. Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, Md.

3. Leidos, Reston, Va.

4. Genomics and Bioinformatics Department, Biological Defense Research Directorate, Naval Medical Research Center, Ft. Detrick, Frederick, Md.

5. Institute of Diagnostic Virology, Freidrich-Loeffler-Institut, Griefswald-Insel Riems, Germany

6. State Office for Agriculture, Food Safety and Fisheries, Rostock, Germany

7. Department of Experimental Animal Facilities and Biorisk Management, Friedrich-Loeffler-Institut, Griefswald-Insel Riems, Germany

8. Institute of Novel and Emerging Infectious Diseases, Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany

9. German Center for Infection Research (DZIF), Hamburg-Luebeck-Borstel-Insel Riems, Griefswald-Insel Riems, Germany

10. Integrated Research Facility at Ft. Detrick, National Institute of Allergy and Infectious Diseases, National Institute of Health, Ft. Detrick, Frederick, Md.

11. Global Health Institute, University of Wisconsin - Madison

Oct 2020 Relatives of Rubella Virus in Diverse Mammals
 
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The article of post #456 states....’first trimester of pregnancy....severe congenital birth defects....causes fetal pathology after transplacental transmission.....cyclops leaf-nosed bats host Plasmodium cyclopsi, an apicocomplexan “bat malaria” parasite....Bennett’s Tree Kangaroo, Dendrolagus bennettianus De Vis, 1886.’

It was at the University of New Mexico, circa 2006, that we sat in on a dissertation defense by a young lady whose thesis was on the placental transmission of Sin Nombre virus. Intrigued, badger mentioned Wakaleo vanderleuri, apparently a (double-uterine [italics]), saber-toothed marsupial lion (thylacoleonid) found at the Etadunna Formation, Australia.

Another Wakaleo species was found at the Miocene Alcoota fossil beds, near Alice Springs:

2015 Miocene Alcoota Wakaleo

Thus, Kangaroo Well fossil beds should link Plasmodium infection in Australian placental-marsupial species:

Bullock Creek, Northern Territory

Next, we link Rubiviruses (Rubella) to coronaviruses via the pharmacokinetics of hydroxychloroquine.
 
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Before linking hcq to rubiviruses, here are shown some geographic links between Homo sapiens and Wakaleo near Etadunna

Etadunna Station
’....During 1879, a Post Office was opened at Kopperamanna and John Neaylon called in delivering the mail and supplies on his way from Marree to Birdsville.’

The Marree Man: Who Put This 2-Mile Long Drawing in the Australian Desert?
 
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First linking rubiviruses to coronaviruses:

’5. Arterivirus EAV is a ‘Mini’ Coronavirus: The Birth of the Nidovirales
Shortly after finishing analysis of BEV, the group led by Eric Snijder described the genome organization of arterivirus EAV. At that time, this virus, together with alphaviruses and rubiviruses was considered to be part of the togavirus family. Although EAV was shown to have distinct virion morphology and a genome size approximately twice as small as that of an average coronavirus genome, it proved to share numerous features with coronaviruses.’
(Gorbalenya, Big Nidovirus Genome, The Nidoviruses: Coronaviruses and Arteriviruses)

Rubella linking Australia:

’....The virus has teratogenic properties and is capable of crossing the placenta and infecting the fetus where it stops cells from developing or destroys them....In 1940, there was a widespread epidemic of rubella in Australia. Subsequently, ophthalmologist Norman McAllister Gregg found 78 cases of congenital cataracts in infants and 68 of them were born to mothers who had caught rubella early in pregnancy. Gregg published an account, Congenital Cataracts Following German Measles in the Mother, in 1941....and notcied that, the earlier the mother was infected, the worse the damage was.’
 
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Chloroquine’s traditional use in malaria compares with the timing in rubella infection during early pregnancy, recalling the ‘bat malaria’ of cyclops (above), a time-window is revealed in this important Italian study:

1996 Instituto Pasteur, Rome / Chloroquine Treatment of Rubella
’....These drugs were exerting their inhibitory activity at penetration....If treatment was performed for at least 9 hours after infection.’
 

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