COVID-19’s Biological Politics


Gold Member
Oct 22, 2016
We continue the history and biology of COVID-19, on occasion showing the absurdities of categorization, which should remain a pathology of Homo sapiens rather than science. The trajectory, then, is political by default.

For instance, a political point is that COVID-19 biology in nature has been disregarded while at the same time, epidemiologists such as Fauci, Foege, and Redfield, have spoke little about the obvious COVID-19 reservoir in nature. This mysterious reservoir, similar to vectors of Ebola, holds clues and secrets to the coronavirus genome. By default, the unknown reservoir‘s genome will undoubtedly link to cancer biology.

Antibody therapy links COVID-19 to other medical pathologies, including cancer. Forthcoming, we’ll take a closer look at REGN technology as it relates to COVID-19 and childhood cancer, a universally fatal cancer, while mapping out comparable mutations in both.
Trump is on the cutting edge of C19 history as REGN tech is circulating in his system. The politics continue here:

NEJM Votes Trump Out
NEJM politicizes C19 biology while it criticizes politicization elsewhere. More scientific are the stats of the 212,000 as to any underlying conditions, genomic susceptibilities, lifestyles that would encourage transmission, etc.

Of interest would be Pelosi’s (physiological [italics]) reaction to Trump’s REGN antibodies. From another thread, we know that Ruth Ginsburg’s pancreatic cancer links to both REGN antibodies and the ACVR1 gene. When we link a childhood cancer, the FOP/ACVR1 assemblage links to it:

Lessons Learned from FOP
’ACVR1 encodes ALK2 with residues affected identical to those that, when mutated in the germline, give rise to the congenital malformation syndrome fibrodysplasia ossificans progressiva (FOP), resulting in the transformation of soft tissue into bone. This unexpected link points toward the importance of developmental biology processes in tumorigenesis and provides an extensive experience in mechanistic understanding and drug development, hard-won by FOP researchers to pediatric neurooncology....These tumors are universally fatal with a median overall survival of 9-12 months....a change of lysine to methionine at position 27 on the histone tail (K27M). Remarkably, such mutations have not been identified in any other cancer type, but are also found in approximately 50% of thalamic GBM.
Classical cases of FOP harboring the R206H mutation may be diagnosed at birth by a signature malformation of the great toes....
therapeutic antibodies appear unsuitable as the activating mutations found in ALK2 affect only the cytoplasmic portion of the receptor. Much effort therefore has focused on small molecule inhibitors that can target the intracellular kinase activity of the rogue ALK2 protein.’

It is now possible to begin comparing COVID-19 genome mutations.
The current goal is to connect the region(s) Trump’s antibody therapy targets to mutations in those regions. There is Chinese difference between the European mutation which arose around Feb 2020: D614G. With very few examples of this mutation in China, the origin is unknown.

Trump’s REGN-COV2 very likely targets this region, which is an area of interest in the receptor binding domain (RBD) of the COVID-19 spike protein. We will copy both the SARS-CoV-2 and SARS-CoV for comparison, which is a biological expression of C19’s evolution. USMB software may not align these sequences for easy inspection, and may require manual alignment:

SARS-CoV followed by SARS-CoV-2
V I T P G T N A S S E V A V L Y Q d V N C T D V S T A I H A D Q L T P A W R I Y S T G N
V I T P G T N T S N Q V A V L Y Q d V N C T E V P V A I H A D Q L T PT W R V Y S T G S

Uncapitalized ‘d’ is position 614.
Shortly we will post the countries and their ratios for this mutation for those who better know their genomic relationships. The study above states
‘In addition to the Netherlands, Switzerland, and France, our data indicate that the D614G sub-strain is frequently detected in Brazil, Finland, and Belgium. However, given the small sample size, it is hard to ascertain whether D614G is the dominant strain in these countries. A recent report corroborated our findings of high prevalence of D614G in Europe. Within the analyzed patient cohort, the variant was first observed in EPI_ISL 406862, collected on 28 Jan 2020, in a sample from Germany. Subsequently, the variant was detected in EPI_ISL 412982, collected on 7 Feb 2020, in a sample from Wuhan, China. Notably, these two samples do not share common variants besides p.D614G. It is unclear whether the variant emerged in China and disseminated to Europe or this variant emerged independently in China and Europe. Intriguingly, in our data the D614G variant was detected only in 2 out of 151 Chinese patients analyzed.’
The numbers of occurrence for the D614G mutation for those who already know something about their familial genes:

Netherlands 66
Switzerland 29
France 21
UK 12
Brazil 8
Belgium 7
Finland 6
Portugal 2
Italy 2
Ireland 2
Germany 2
Denmark 2
China 2
Russia 1
Mexico 1
Luxembourg 1
Georgia 1
Chile 1
The World’s leading medical journal, NEJM, has just gone rabidly fascist against the Trump administration. An excellent example of COVID-19 biological politics, the discourse includes 35 un-named people who signed while playing the race card:

‘Let’s be clear about the cost of not taking even simple measures. An outbreak that has disproportionately affected communities of color has exacerbated the tensions associated with inequality.’

Black doctors recently also went preemptively racist in arguing for unity in vaccine politics based on blacks’ fear or superstition, linking back to Ebola politics on Africa. NEJM makes the blunder of saliently introducing politics into COVID-19 epidemiology and biology. The journal fails to add that b.l.m./a.n.t.i.f.a were busy destroying American infrastructure while the virus raged. This indeed would exacerbate immune problems for these scapegoat-victims of Marxist-racist violence, by the introduction of fear and terror. Especially weakened would be elderly contemplating these insane events, so NEJM fails to address medical issues related to the pandemic in the U.S.
Here are shown some aspects of Trump’s REGN-COV2 that link to the receptor binding domain sequences we have already posted in this thread:

Trump’s Treatment Explained
‘....REGN10933 binds to the RBD from the top, REGN10987 only binds to the front or the lower left side of the RBD....and has little to no overlap with the ACE2 binding site.’
Biological politics move to Wisconsin, the worst-hit US state. The argument is, not surprisingly, politics, though the CO2 compromise of mask wearing should also figure into the discussion. Later today we’ll try to address the issue.
Fauci gets it backwards in the video (D614G, rather than G614D), though what we’re interested in is whether or not this prominent C19 mutation affects hypoxia-inducing factor 1 (HIF-1) for our current investigation regarding mask wearing and CO2. The mutation question begins at time point 6:45 in the video:

Biologically political, Chris Christie has just been released from the hospital after having received Trump’s REGN-COV2, and has received a congratulatory phone call from King Abdullah of Jordan.

On the hypoxia trajectory, we note what is still baffling to physicians:

After having viewed the Fauci video above, we did a Pubmed search in an attempt to link Fauci’s D614G C19 (Aspartic acid-to-glycine) mutation to hypoxia-inducible factor 1 (HIF-1):

HIF-1 and Glycine yields 119 references. HIF-1 and aspartic acid yields 44 references. However, adding the search ‘hif-1 aspartic’ yields 113 references. Thus, there are few clues at this point to reveal what COVID-19 was “thinking” when it went from aspartic acid to glycine to increase its affinity to the ACE2 receptor.
We next recalled Zelenko’s tripartite COVID-19 treatment, hydroxychloroquine, azithromycin, and zinc. Trump received zinc, Remdesivir, and REGN-COV2. At this time, it’s difficult to say if Remdesivir is replacing the hcq or azithromycin. Nevertheless, when we link HIF-1 to azithromycin, we come up with Christie’s link to REGN-COV2: asthma. It happens due to rapamycin’s link to both REGN-COV2 and rapamycins target, mTOR.

REGN-2477 / Rapamycin/ Therapeutic Advances

We mentioned REGN-2477 in posts # 1,068 & #1,079 of the snake meant thread.

Christie’s asthma meets Zelenko’s Azithromycin:
Asthma / Azithromycin / HIF-1

Coronavirus Dysregulation of AKT/mTOR/HIF-1
Because HIF-1 directly links to SARS-COV-2, one would question an individual’s genomic ability to adopt to increased CO2 in mask wearing, especially for a virus that has gained, only since January 2020, an increased ability to bind to ACE2.
In the video, the priest comes on to introduce Fauci, who then misinterprets the COVID-19 mutation, D614G. The viewer would think that this is current information, though the mutation occurred between the last week in Jan 2020 and the first week of Feb 2020 in two countries, Germany and China.

Understanding adaptive immunity to SARS-CoV-2 is important for vaccine development, interpreting coronavirus disease 2019 (COVID-19) pathogenesis, and calibration of pandemic control measures. Using HLA class I and II predicted peptide “megapools,” circulating SARS-CoV-2-specific CD8+ and CD4+ T cells were identified in ∼70% and 100% of COVID-19 convalescent patients, respectively. CD4+ T cell responses to spike, the main target of most vaccine efforts, were robust and correlated with the magnitude of the anti-SARS-CoV-2 IgG and IgA titers. The M, spike, and N proteins each accounted for 11%–27% of the total CD4+ response, with additional responses commonly targeting nsp3, nsp4, ORF3a, and ORF8, among others. For CD8+ T cells, spike and M were recognized, with at least eight SARS-CoV-2 ORFs targeted. Importantly, detected SARS-CoV-2-reactive CD4+ T cells in ∼40%–60% of unexposed individuals, suggesting cross-reactive T cell recognition between circulating “common cold” coronaviruses and SARS-CoV-2.we

A study by Monash Biomedicine Discovery Institute (BDI) expands the understanding of the molecular pathways that control T cell function and survival and how it relates to declining T cell immunity in the elderly.

The findings, published in Nature Communications, led by Monash BDI's Professor Nicole La Gruta and Dr. Kylie Quinn (formerly of Monash University BDI, now Vice-Chancellor's Research Fellow at RMIT University), outline that the increased metabolism of T cells observed with advanced age was an indication that they were working harder merely to survive.

This contradicts previous knowledge, which suggested an increased metabolism was indicative of T cell function, and will have implications for the development of targeted interventions such as vaccines or immunotherapies to treat age-related immune dysfunction.

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