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    • Mon, Jul 13, 2020 - 11:57am

      #4
      TurquoiseRose

      TurquoiseRose

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      D614G – No evidence for increased human transmission

    Reply to tatagirl RE:  D614G – No evidence for increased human transmission

    ORF3c has a new stop codon hitchhiking with Spike-D614G the dominant strain “G“ Clade

    https://www.biorxiv.org/content/10.1101/2020.05.21.109280v1.full.pdf

    Do OLG’s (Overlapping genes) Increase transmissibility?

    ORF3c ->predicted protein of 238 amino acids; a membrane protein with 3 transmembrane regions.

    ORF3c gained a new stop codon (G25563U) that rose in frequency; 401 sequenced samples demonstrate this mutation in multiple hosts.

    New ORF3c stop codon hitchhiked early with haplotype 241U/3037U/14408U/23403G (Spike-D614G), ->drives European + world spread.

    Results liken ORF3c to other important viral accessory genes recombined, lost, split, or truncated before or during outbreaks, including ORF3b + ORF8.

    OLGs deserve considerably more attention, their rapid evolution may be more important than is currently appreciated in the emergence of zoonotic viruses.

    Epistatic network in SARS-CoV-2 genome

    https://www.biorxiv.org/content/10.1101/2020.04.10.035964v1.full.pdf

    Another concept harder to ferret out-  Do neighboring genes affect each other?

    Coevolving pair codons
    involving sites evolving under positive selection at different regions of SARSCoV-2 genome are shown with stars, suggesting selection of these sites may be the result of epistasis (Neighboring genes affecting each other).

     

     

    • Mon, Jul 13, 2020 - 10:08am

      #2
      TurquoiseRose

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      D614G – No evidence for increased human transmission

    Perhaps he missed this paper ->

    D614G mutation in the SARS-CoV-2 spike protein
    reduces S1 shedding & increases infectivity by 9X’s compensating for furin cleavage site From Scripps.

    https://www.biorxiv.org/content/10.1101/2020.06.12.148726v1.full.pdfV

    Viruses with Spike-G614 were 9X’s more infectious in cell culture  than those without the mutation.

    Ø  Mutation markedly increased functional spikes on viral surface by 4-5 times.

    Ø   Spikes are what allow the virus to bind to + infect cells via ACE2 receptors.

    Ø  D614G, provides greater flexibility to the spike’s “backbone” allowing newly made viral particles to navigate from the producer cell to target cell fully intact, with less tendency to fall apart prematurely.

    This conserves the S1 piece-> so there are more copies

    • Sat, Jul 11, 2020 - 11:13pm

      #3
      TurquoiseRose

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      Furin cleavage site may not have been deliberately engineered.

    That is true that furin sites have been found in nature. Also in 2 species of pangolins.

     

    It is also true that labs in the US, Japan, and most recently China have published placing furin cleavage sites in viruses.  Using CRISPR there is no residue or sign of insertion.

    see: he also gives references- I while back I did a PubMed search and found more papers that he did not site. They were American.

    https://medium.com/@yurideigin/lab-made-cov2-genealogy-through-the-lens-of-

    gain-of-function-research-f96dd7413748

    • Wed, May 13, 2020 - 11:58am

      #2
      TurquoiseRose

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      Could Wuhan Strain Not Be What Hurt Wuhan?

    I also noticed 3 strains A Wuhan, B (Europe), C  -Italy, Singapore,

    Type A is closest to the one found in bats and pangolins and has two sub-clusters

    One sub-cluster linked to Wuhan and the other is common in US and Australia

    Type B is derived from type A and has become the most prevalent in Wuhan

    Type C is the ‘daughter’ of type B and was spread to Europe via Singapore

    https://www.biorxiv.org/content/10.1101/2020.03.15.991844v3

    TYPE A – T29095C subclusters
    T-allele->Ancestral genome found  in 4 Southern Coastal Chinese, Slight mutations in 2 Japanese + 2 Americans (lived in Wuhan)
    C-allele – long mutational branches +5 from Wuhan, 2 in the ancestral node, + 8 East Asians from China + adjacent countries. Half (15/33) are found outside East Asia, mainly in the US + Australia.
    TYPE B- derived from A by 2 mutations: the synonymous mutation(no change) T8782C + nonsynonymous mutation C28144T changing  leucine -> serine in EAST ASIANS.
    TYPE C differs from type B by nonsynonymous mutation G26144T which changes  glycine -> valine. Major European type (n = 11), in France, Italy, Sweden+ England, California + Brazil. Not in Chinese sample, Found in Singapore (n = 5) + Hong Kong, Taiwan,+ South Korea.
    https://www.pnas.org/content/early/2020/04/07/2004999117

    D614G mutation is increasing and is now taking over- see link below

    https://www.biorxiv.org/content/10.1101/2020.04.29.069054v1

     

     

    • Mon, May 11, 2020 - 09:56pm

      #3
      TurquoiseRose

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      Math+ protocols

    Link to MATH+ Protocol

    https://covid19criticalcare.com/wp-content/uploads/2020/04/MATHPressRelease.pdf

    • Mon, Apr 06, 2020 - 09:55am

      #3
      TurquoiseRose

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      FROM NYC ICU: DOES COVID-19 REALLY CAUSE ARDS?

    Covid-19 attacks the hemoglobin and may be mechanism causing poor oxygenation

    ±Covid- 19 Captures the Porphyrin to Inhibit Human Heme Metabolism
    ± ORF8 and surface glycoprotein could bind to the porphyrin

    ±orf1ab, ORF10, and ORF3a proteins could coordinate attack the heme on the 1-beta chain of hemoglobin to dissociate the iron to form the porphyrin
    ±attack will cause less +  less hemoglobin that can carry oxygen and carbon dioxide

    ±Extreme poisoning of lung  cells
    ±Inflammation due to the inability to exchange CO2 + O2 frequently resulting in ground-glass-like lung images
    ±Mechanism interferes with heme anabolic pathway = is expected to result in human disease

    ±Chloroquine could prevent orf1ab, ORF3a, and ORF10 from attacking heme to form porphyrin, + inhibit the binding of ORF8 and surface glycoproteins to porphyrins .
    ±This relieves symptoms of respiratory distress. Favipiravir could inhibit the envelope protein + ORF7a protein bind to porphyrin, prevent the virus from entering host cells, and catching free porphyrins.  See below Preprint:

    https://chemrxiv.org/articles/COVID-19_Disease_ORF8_and_Surface_Glycoprotein_Inhibit_Heme_Metabolism_by_Binding_to_Porphyrin/11938173

    • Sun, Apr 05, 2020 - 01:26pm

      #2
      TurquoiseRose

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      Reply To: FROM NYC ICU: DOES COVID-19 REALLY CAUSE ARDS?

    Acetazolamide, Nifedipine and Phosphodiesterase Inhibitors: Rationale for Their Utilization as Adjunctive Countermeasures in the Treatment of Coronavirus Disease 2019 (COVID-19) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7096066/

    Thought this was already posted- see this article as tables do not paste well.
    Similar patterns of pulmonary disease between HAPE and COVID-19

    HAPE: High altitude pulmonary edema; COVID-19: Coronavirus disease 2019;
    In light of this, a countermeasure that has been shown to be effective in high altitude illness is Acetazolamide.

    Sample medications and dosages utilized in high altitude illness and HAPE

    HAPE: High altitude pulmonary edema
    Acetazolamide  250 mg every 12 hours
    Nifedipine 30 mg extended release every 12 hours
    Sildenafil 20-50 mg every 8 hours
    Tadalafil 10 mg every 12 hours

    +++++++++++++++++++++

    Take away from video- using the wrong ventilator pressures will cause more harm than good with catastrophic iatrogenic lung injury.

    This flawed Algorithm is widely circulated both nationally and internationally and is likely to be difficult to change.

    He appears to be a maverick seeing harm and alerting us, as were the researchers publishing that Covid -19 was looking like HAPE and could perhaps be better served by trying meds that were already known to benefit HAPE (a failure of oxygenation).

    ++++++++++++++++++++++++++

    To tie this into Catherine Fitts -Plandemic, where she considers the possibility of  another variable as to why so many have flu symptoms.

    A.   4-5G has been, by themselves are associated causing an increase in flu-like symptoms.

    B.  5G has apparently also been associated with biological interference with oxygenation  https://www.takebackyourpower.net/critical-examination-of-the-coronavirus-5g-connection/

    1) 60-GHz oxygen band: Precise experimental profiles and extended
    absorption modeling in a wide temperature range [2011, Journal of Quantitative Spectroscopy & Radiative Transfer]
    2) Evaluation of the Potential Biological Effects of the 60-GHz Millimeter Waves Upon Human Cells [2009, IEEE]
    3) Fixed Wireless Communications at 60GHz Unique Oxygen Absorption Properties [2001, Shigeaki Hakusui, Harmonix Corporation]

    • Thu, Apr 02, 2020 - 08:04am

      #2
      TurquoiseRose

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      IT’S A MIRACLE –No this is

    McMichael seeks FDA OK for COVID-19 cure
    https://www.timesjournalonline.com/article.asp?id=104957

    • Sat, Mar 21, 2020 - 12:13pm

      #6
      TurquoiseRose

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      Let’s look at some other numbers

     

    This site is trying to keep updated ever 2 days.  It has some other interesting datasets to help us figure this out.

    https://medium.com/six-four-six-nine/evidence-over-hysteria-covid-19-1b767def5894

    • Mon, Mar 16, 2020 - 05:44pm

      #2
      TurquoiseRose

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      “Op-Ed: Does the 2019 Coronavirus Exist?”

    Investigative reporter, Jon Rappaport has similar views, see his blogs:  https://nomorefakenews.com/

    COV death: Five-thousand-year-old man had two hundred diseases, was on three hundred toxic meds

    ++++++++++++

    I guess all we know for sure is that people have died.   I think back in his blogs another reporter found out the Swine flu numbers were not accurate.  The swine flu tests were all coming back negative.  So they just put “flu” cases in that category.  I am not an expert in any of this.  Why would Italy and Spain be lying?  Everybody has their opinions.

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