Pfizer COVID-19 vaccine linked to rare blood disease - Israeli study

We’re placing this here for the alpha-sarcin trajectory, and since it also includes luciferase and permeability, luciferase somewhere having been mentioned at USMB. Poliovirus makes for more permeability to alpha-sarcin, a protein toxin. VSV, also an ebola-based vaccine virus, is also implicated. Cardiovirus is a Picornaviridae, like polio.

Permeability to Alph Sarcin in Virus-Infected Cells / Encephalomyocarditis

But chloroquine does not prevent poliovirus entry, whereas at first it was thought that it did. No doubt, CIA, MI6, and other intelligence agencies are aware of sarcin use during a bioweapon attack:

Spain 1987 / Poliovirus / Chloroquine Blocks Co-Entry of Alpha-Sarcin
 
We're bringing this thread forward for current Russian news on the biolabs. There is already a mosquito/biolab thread that has been placed in this forum, which links to the Bulgarian journalist mentioned in this thread (Dilyana).

 
Actually, it was placed in Conspiracy:

7 Jul 2022
'....to study ebola....the research was to be carried out....in Odessa. Bundeswehr professionals paid particular attention to the Congo-Crimean fever pathogen....particular attention to fatal cases, as it allows the virus strains with maximum pathogenicity and virulence for humans to be extracted from the dead individuals.'
 
We have already posted (USMB search: Neophocaena) on the Yangtze finless porpoise as suspected intermediate host of SARS-CoV-2. We have already posted (USMB search: Withania) on the abortifacient chemistry which links Ben Franklin's abortifacient, Pennyroyal, against SARS-CoV-2.

We have already posted on the de-activation of coronaviruses by chloroquine (USMB search: Blau and Holmes, International Symposium, Philadelphia, 2000). We have already posted on the activation of HOX genes during differentiation and linked this activation to chloroquine:
'....chloroquine, Liu, et al, Wuhan Institute of Virology:
....'

An important link will be the bat viruses collected in Laos, with particular reference to BANAL-236 from Rhinolophus marshalli (northern Laos, 2020). This bat virus links to Edward C. Holmes (Australia), whom Edward Hooper (AIDS Origins page) has already mentioned, Holmes having co-authored papers with Yongzhen Zhang.

Note SARS-CoV-2 virus announced in Jan 2020.

Yongzhen Zhang
'....along with Edward C. Holmes, U. of Sydney, was awarded the 2021 General Symbiont prize.'

Edward C. Holmes / Rhinolophus marshalli
'....of most note, five SARS-CoV-2-related coronaviruses were recently identified in these Rhinolophus species in Laos (R. malayanus, R. pusillus, R. marshalli), three of which grouped closely with human SARS-CoV-2 on phylogenetic trees and possessed a receptor binding domain with high sequence similarity to that of SARS-CoV-2 And the ability to bind to human ACE2 receptor.'

Note that the Holmes report is co-authored along with:
'Shenyang Agricultural University, Shenyang, China; State Key Laboratory of Estuarine and Coastal Research, Shanghai; Dept. Of Laboratory Medicine and Pathobiology, University of Toronto, Canada.'

SARS-CoV-2 was reported in the media in Jan 2020. BANAL-236 strain from laotian R. marshalli was mentioned here:

Feb 2020 / Illegal Wildlife Trade in Vietnam

The Neophocaena link mentioned above, links to the evolution of HOX genes. We have already mentioned HOX genes for Guttmacher syndrome and hand-foot-genital syndrome that connect with abortifacient chemistry and we have already posted on Beluga whale coronavirus sequences here at USMB:

Jun 2007 Northeast Ohio University College of Medicine / Evolution of HOX Gene Family in Bats and Dolphins
'....An example of these differing morphologies is illustrated in manus bending in whales vs. bats. The hyperphalangeous flipper of a humpback whale bends at numerous angles to create a smooth arc along the length of a digit, while the elongated digits in wings of bats bend at sharp angles at interrphalangeal joints.
....
Evolutionarily, perhaps hyperphalangy is a functional consequence of having a lift-generating flipper with the greatest pressure on the leading edge surface, as in airfoils.
....
Institute Source and Specimens Studied: Delphinapterus leucas.'

Beluga Whale, Delphinapterus leucas.
 
The above 2007 Northeast Ohio U. Study that mentions the host of Beluga whale coronavirus is referenced in this report:

Adaptive Evolution of HOX Gene Family in Bats and Dolphins
 
Note that the above evolution study of HOX genes is from Kunming. This is not only the city from which Daszak collected the bat virus from Rhinolophus sinicus given to UNC-Chapel Hill's Baric, it is also where both Zhang and Holmes link to zoological institutes; one for Kunming Insititue of Zoology (Zhang attended this institute), and, as Edward Hooper states on his HIV/AIDS blog, Oxford Institute of Zoology.
 
We will attempt to link mid-trimester human sonography findings to the development of Rhinolophus marshalli BANAL-236, above.

Jan 2022 Dept. of Obstetrics and Gynecology, SUNY Brooklyn, New York / Mid-Trimester Sonography / HOXD10 Mutations
 
Above, the 3 Ap 2011 publication for bats and dolphins HOX gene evolution came two weeks before Daszak (Eco Health Alliance) and Shi (Wuhan Inst. Virology) collected the RsSHC014 Kunming virus, which was then given to Baric:

Shi, ZL, Daszak, P. / Rhinolophus sinicus SHC014 Genome
' collection date: 17 Ap 2011.'

Baric, R / Rhinolophus sinicus SHC014 Synthetic Vaccine Construct
'submitted 11 Jun 2021.'
 
The entry for post #225:

Edward C. Holmes, et al / Rhinolophus marshalli
 
Mid-trimester HOXD mutations (post #228) detected by sonography implicates at least two mutations: Omicron N969K (the vaccine-linked mutation) and Omicron D796Y (the "Beluga whale" mutation). So to verify, the question is: "Is Beluga whale coronavirus spike @ position 796 really linked to Omicron mutation D796Y?"
 
OP's report states: 'thrombotic thrombocytopenic purpura....hemorrhage.' Here we link HOXA (HOXA13 = Guttmacher syndrome) and HOXD (absence of mutations [italics]) to thrombocytopenia and lack of radius (which is a limb-development comparable with HOXD10 of Rhinolophus marshalli with known affinity to human ACE2 receptors. Notice the megakaryocyte connection to SARS-CoV-2 autopsies, already posted to USMB:

2002, British Journal of Haematology, Fleischman, et al (U. of Kentucky and VA Medical Center / Oncology Division, Lexington)
Absence of Mutations in the HOXA10, HOXA11 and HOXD11 Nucleotide Coding Sequences in Thrombocytopenia with Absent Radius Syndrome
'Although these studies cannot completely exclude the possibility that the TAR syndrome results from non-coding mutations that effect the level of HOX gene expression in megakaryocytes, mutations in the coding sequences of the HOX genes known to affect radial development are not a common cause of TAR syndrome.'

In reply to the Omicron D796Y mutation, this comparison. Position 796 is not capitalized:

Beluga coronavirus spike, positions 791-800:

F K Y C Y y D D V I

SARS-CoV-2 spike, positions 791-800

T P P I K d F G G F

Thus both amino acids of the Omicron D796Y mutation link to Beluga whale coronavirus spike protein.
 
Linking megakaryocytes at COVID-19 autopsy, was post #667 of 2 Jul 2020:

Here is what Epstein says about TAR:

'p. 668: The features of ATRUS (Amegakaryocytic Thrombocytopenia with Radioulnar Synostosis) include thrombocytopenia at birth and bilateral proximal fusion of the radius and ulna....One child reported with this disorder also had fifth finger clinodactyly. In addition, two unrelated families have been described with adult-onset aplastic anemia in association with radioulnar synostosis.
....
The only genetic defect identified to datе in association with ATRUS is mutation of HOXA11. Thompson and Nguyen described two unrelated families in which the fathers have radioulnar synostosis and transmitted this to four of the five total children. Three of the children also have amegakaryocytic thrombocytopenia, although the fathers both have normal platelet counts. In both of these families, the father and affected children carry a single base-pair deletion in the third helix of the homeodomain of HOXA11 that results in a premature stop codon and is predicted to disrupt DNA binding (Thompson and Nguyen, 2000). This mutation was absent in the mothers and unaffected child, as well as 10 random normal individuals. Furthermore, studies have not detected HOXA11 mutations in patients with TAR (Fleischman et al, 2002). As the genetic basis of ATRUS has been elicited in only two reported cases, it is possible that some individuals with features of this disorder carry mutations in genes other than HOXA11.
....
p. 872: TBX3 and TBX5 and the Ulnar-Mammary and Holt-Oram Syndromes....There are many diagnostic possibilities for individuals who present with limb and heart defects, but only a few of these conditions are relatively common. The most frequent diagnoses that are characterized by a pattern of malformations similar to Holt-Oram syndrome (HOS) are VATER/VACTERL (includes vertebral, anal, cardiac, tracheal, esophageal, radial, renal, and limb anomalies) association, thrombocytopenia and absent radius (TAR) syndrome (OMIM 274000), Fanconi's anemia, Okihiro's syndrome (OMIM126800) and several hand-heart syndromes.

....TAR syndrome can be distinguished from HOS by the presence of a normal or slightly hypoplastic thumb accompanied by severe hypoplasia or aplasia of the radius.'
(Epstein, Inborn Errors of Development: The Molecular Basis of Clinical Disorders of Morphogenesis)
 
Hox genes link to brown adipose tissue (BAT) and cold adaption:

Dec 2021 Tierra del Fuego

Zika and human pregnancy link to the HOX genes of previous posts:

Dec 2021 SARS-CoV-2 Human Pregnancy / Zika / Mycoplasma

Mycoplasma is key in co-infections with viruses:

Sendai / BAT

The SARS-CoV-2 connection is the severity of infection. Mycoplasma co-infection with canine respiratory coronavirus:

These reports link to Beluga whale living its life under the sea ice while being infected with its own coronavirus, and overweight diabetic humans infected with SARS-CoV-2.
 
It was surprising to find that Kennedy (The Real Anthony Fauci) had already made a mycoplasma connection to Fau Chi and HIV/AIDS.

For readers to jump ahead in lieu of forthcoming excerpts, there is a youtube video and Kennedy gives the timepoint:

Brett Leung, "Knowledge Matters, House of Numbers - Anatomy of an Epidemic," YouTube video, 19 Ap 2009, 00:47:33
 
Kennedy on the mycoplasma connection:

'Mycoplasma. Dr. Shyh-Ching Lo, the Chief Researcher in charge of AIDS programs for the Armed Forces Institute of Pathology, was one of the many researchers baffled by Anthony Fauci's unconventional claim that antibodies - heretofore the signal of a robust immune response - should, uniquely with HIV, instead be the signal for impending death. That was a bridge too far for Dr. Lo: he took the conventional position that the presence of antibodies to HIV - far from being a sign of doom - is proof that the body has coped successfully with the virus.

"There is no good explanation for why and how the virus breaks out of the antibody protection," complained Dr. Lo. "I'm just saying that HIV plays no role in AIDS- the data shows a clear correlation with disease." He recited the mandatory disclaimer: "But AIDS is much more complicated than HIV."

In 1986, Dr. Lo announced that he had detected a previously unknown organism in cells taken from AIDS patients. Dr. Lo said that he believed the new organism, a bacterium-like creature known as mycoplasma, worked with HIV to cause AIDS. Dr. Lo coulr not find the organism in any healthy individuals. When he injected his mycoplasma into four silvered leaf monkeys, three quickly developed low-grade fevers. All four lost wight and died between seven and nine months of infection. During autopsy, Dr. Lo found mycoplasma in their brains, livers and spleens. That does not happen with HIV.'
(Kennedy, The Real Anthony Fauci, pp. 234-5)
 
Here we track the ACE2 link to CFS (chronic fatigue syndrome), as Kennedy continues:

'Dr. Lo also found the mycoplasma, dubbed Mycoplasma incognitus, in the damaged tissue of six HIV-negative human beings - perhaps CFS sufferers - who had died with suppressed immune systems after suffering from suspiciously AIDS-like symptoms. For nearly three years, mainstream medicine the captive mainstream and science media dutifully ignored Dr. Lo's research. A dozen scientific journals turned down Shyh-Ching Lo's studies for publication before the Journal of Tropical Medicine agreed to print his findings. Despite his impressive credentials and his prestigious post as top military scientist, Dr. Lo's attempts to find funding failed.

Dr. Lo's research posed a unique annoyance for Dr. Fauci. Because he was a top military doctor with his own laboratory, he could not be easily dismissed, bullied or defunded. Then in December, 1989, Dr. Fauci opted to meet this threat from the military with a direct frontal assault. NIAID dispatched a dozen of Dr. Fauci's most skeptical specialists to investigate Dr. Lo's data. Dr. Fauci flew his leading experts in AIDS and other infectious diseases to San Antonio, Texas, for the confrontation, expecting to obliterate Dr. Lo and to discredit his theory.

Dr. Fauci's panel members quizzed Dr. Lo mercilessly for three days before surrendering to the conclusion that Dr. Lo had made a momentous discovery. "The documentation was absolutely solid," said Joseph Tully, head of mycoplasma programs for NIAID. The newly converted NIAID participants formally recommended further study of the link between the mycoplasma and AIDS, and experiments with drugs that could kill the new microbe.

The recommendation apparently displeased Dr. Fauci. "We have not been pulled Into the AIDS programs in any real way," Tully complained in 1990. Thirty-five years after Dr. Lo's initial announcement, NIAID has still funded no research on Dr. Lo's mycoplasma hypothesis.'
(Kennedy, op cit p. 235)
 
Aug 2021 Germany, Poland, Spain, Portugal, Chile, UK, Canada / Chronic Fatigue Syndrome / ACE2 Receptor
 

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