View All Posts: WILLSAN

luki said:
Yes, that was why Frontier Science News, who Kory asked to publish his initial review, rejected the paper. It was basically a free add for his treatment. That said Gates foundation could prove Kory right.
Further, the authors promoted their own specific ivermectin-based treatment which is inappropriate for a review article and against our editorial policies.
“In our view, this paper does not offer an objective nor balanced scientific contribution to the evaluation of ivermectin as a potential treatment for COVID-19.
https://blog.frontiersin.org/2021/03/02/2-march-2021-media-statement/

luki said:I read the transcript of the testimony he gave in December. 2hrs a bit long to watch He is flogging his specific regimen of care with the drug and unhappy Gates may say another more effective.

cowie said:
Not a great endorsement for the quality of UKSM Competitor's that.

luki said:I was reading about this and the dose size used in treatment is huge (read potentially liver damaging.) It's an over the counter drug and there is a concern people are taking it like a daily multivitamin in the belief this will prevent catching Covid (as was the case with interferon.) They be better off using a mouth wash and washing hands more regularly! It's also available for animals which is being sold online here.

EMA are waiting for the results of the Gate foundation clinical trial next month. Hungary and Slovakia are using in hospital. Not sure it's a cover up when Gates foundation are actively testing.

Good new if it does work, it's widely produced and very cheap. A pack of 12 is €6. Not sure if that whole pack is a dose for Covid treatment

Mikeneto said:Group 1 and group 5 are the group of death.

Rick said:Of course not. Doesn't fit your narrative.

Rick said:
One of the many things mentioned in this roundup of what evidence the is and isn't.
http://www.sciencealert.com/the-lab-leak-theory-of-covid-19-ma...
Spoiler alert: it ain't evidence for what you want it to be evidence for.

Billytheold said:

I said:'furin cleavage site'
from 15:43:

https://onlinelibrary.wiley.com/doi/full/10.1002/bies.202000240

very long analysis and history of coronavirus GOF research which I posted earlier in the thread:
https://yurideigin.medium.com/lab-made-cov2-genealogy-through-the-lens-of-gain-of-function-research-f96dd7413748

3) The furin cleavage site.

The furin cleavage site is a minute part of the virus’s anatomy but one that exerts great influence on its infectivity. It sits in the middle of the SARS2 spike protein. It also lies at the heart of the puzzle of where the virus came from.
The spike protein has two sub-units with different roles. The first, called S1, recognizes the virus’s target, a protein called angiotensin converting enzyme-2 (or ACE2) which studs the surface of cells lining the human airways. The second, S2, helps the virus, once anchored to the cell, to fuse with the cell’s membrane. After the virus’s outer membrane has coalesced with that of the stricken cell, the viral genome is injected into the cell, hijacks its protein-making machinery and forces it to generate new viruses.
But this invasion cannot begin until the S1 and S2 subunits have been cut apart. And there, right at the S1/S2 junction, is the furin cleavage site that ensures the spike protein will be cleaved in exactly the right place.
The virus, a model of economic design, does not carry its own cleaver. It relies on the cell to do the cleaving for it. Human cells have a protein cutting tool on their surface known as furin. Furin will cut any protein chain that carries its signature target cutting site. This is the sequence of amino acid units proline-arginine-arginine-alanine, or PRRA in the code that refers to each amino acid by a letter of the alphabet. PRRA is the amino acid sequence at the core of SARS2’s furin cleavage site.
Viruses have all kinds of clever tricks, so why does the furin cleavage site stand out? Because of all known SARS-related beta-coronaviruses, only SARS2 possesses a furin cleavage site. All the other viruses have their S2 unit cleaved at a different site and by a different mechanism.
How then did SARS2 acquire its furin cleavage site? Either the site evolved naturally, or it was inserted by researchers at the S1/S2 junction in a gain-of-function experiment.
Consider natural origin first. Two ways viruses evolve are by mutation and by recombination. Mutation is the process of random change in DNA (or RNA for coronaviruses) that usually results in one amino acid in a protein chain being switched for another. Many of these changes harm the virus but natural selection retains the few that do something useful. Mutation is the process by which the SARS1 spike protein gradually switched its preferred target cells from those of bats to civets, and then to humans.
Mutation seems a less likely way for SARS2’s furin cleavage site to be generated, even though it can’t completely be ruled out. The site’s four amino acid units are all together, and all at just the right place in the S1/S2 junction. Mutation is a random process triggered by copying errors (when new viral genomes are being generated) or by chemical decay of genomic units. So it typically affects single amino acids at different spots in a protein chain. A string of amino acids like that of the furin cleavage site is much more likely to be acquired all together through a quite different process known as recombination.
Recombination is an inadvertent swapping of genomic material that occurs when two viruses happen to invade the same cell, and their progeny are assembled with bits and pieces of RNA belonging to the other. Beta-coronaviruses will only combine with other beta-coronaviruses but can acquire, by recombination, almost any genetic element present in the collective genomic pool. What they cannot acquire is an element the pool does not possess. And no known SARS-related beta-coronavirus, the class to which SARS2 belongs, possesses a furin cleavage site.
Proponents of natural emergence say SARS2 could have picked up the site from some as yet unknown beta-coronavirus. But bat SARS-related beta-coronaviruses evidently don’t need a furin cleavage site to infect bat cells, so there’s no great likelihood that any in fact possesses one, and indeed none has been found so far.
The proponents’ next argument is that SARS2 acquired its furin cleavage site from people. A predecessor of SARS2 could have been circulating in the human population for months or years until at some point it acquired a furin cleavage site from human cells. It would then have been ready to break out as a pandemic.
If this is what happened, there should be traces in hospital surveillance records of the people infected by the slowly evolving virus. But none has so far come to light. According to the WHO report on the origins of the virus, the sentinel hospitals in Hubei province, home of Wuhan, routinely monitor influenza-like illnesses and “no evidence to suggest substantial SARSCoV-2 transmission in the months preceding the outbreak in December was observed.”
So it’s hard to explain how the SARS2 virus picked up its furin cleavage site naturally, whether by mutation or recombination.
That leaves a gain-of-function experiment. For those who think SARS2 may have escaped from a lab, explaining the furin cleavage site is no problem at all. “Since 1992 the virology community has known that the one sure way to make a virus deadlier is to give it a furin cleavage site at the S1/S2 junction in the laboratory,” writes Dr. Steven Quay, a biotech entrepreneur interested in the origins of SARS2. “At least eleven gain-of-function experiments, adding a furin site to make a virus more infective, are published in the open literature, including [by] Dr. Zhengli Shi, head of coronavirus research at the Wuhan Institute of Virology.”

Fauci Was Told Early on That Wuhan Coronavirus Looked 'Engineered'

New emails obtained by Buzzfeed through a Freedom of Information Act show National Institute of Health Director Dr. Anthony Fauci was told by NIH scientist Kristian Andersen on January 31, 2020 that Wuhan coronavirus looked "potentially engineered." In other words, it was manipulated in a lab through gain of function research.

"On a phylogenetic tree the virus looks totally normal and the close clustering with bats suggest that bats serve as the reservoir. The unusual features of the virus make up a really small part of the genome so one has to look really closely at all the sequences to see that some of the features (potentially) look engineered," Andersen said.

And yet, that's not what he said publicly as he rejected the possibility of a lab leak in interviews, during testimony to Congress and during official White House Task Force briefings. On April 18, 2020, three months after being told the virus looked engineered, Fauci told reporters at the White House, unequivocally, it didn't come from a lab. Most of the media then reported his remarks as "debunking" a conspiracy theory.

Mikeneto said:Day One

Loading Medley (all groups), Squat lift (groups 1&3), Deadlift (groups 2,4&5).

Day 2

Fingals finger (groups 1,4&5), Train Pull (groups 2&3).

Day 3

Overhead medley (all groups), Pick axe hold (all groups, winner of groups goes straight to final), Stone off (for final spot in final between person in second and third).

CONCLUSIONS AND OUTLOOK

On the basis of our analysis, an artificial origin of SARS-CoV-2 is not a baseless conspiracy theory that is to be condemned[66] and researchers have the responsibility to consider all possible causes for SARS-CoV-2 emergence. The insertion of human-adapted pangolin CoV RBD obtained by cell/animal serial passage and furin cleavage site could arise from site-directed mutagenesis experiments, in a context of evolutionary studies or development of pan-CoV vaccines or drugs. A recent article in Nature[67] affirms that a laboratory origin for SARS-CoV-2 cannot be ruled out, as researchers could have been infected accidentally, and that gain-of-function experiments resulting in SARS-CoV-2 could have been performed at WIV. Genetic manipulation of SARS-CoV-2 may have been carried out in any laboratory in the world with access to the backbone sequence and the necessary equipment and it would not leave any trace. Modern technologies based on synthetic genetics platforms allow the reconstruction of viruses based on their genomic sequence, without the need of a natural isolate.[68]

Conclusion
More than a year after the initial documented cases in Wuhan, the source of SARS-CoV-2 has yet to be identified, and the search for a direct or intermediate host in nature has been so far unsuccessful. The low binding affinity of SARS-CoV-2 to bat ACE2 studied to date does not support Chiroptera as a direct zoonotic agent. Furthermore, the reliance on pangolin coronavirus receptor binding domain (RBD) similarity to SARS-CoV-2 as evidence for natural zoonotic spillover is flawed, as pangolins are unlikely to play a role in SARS-CoV-2′s origin and recombination is not supported by recent analysis. At the same time, genomic analyses pointed out that SARS-CoV-2 exhibits multiple peculiar characteristics not found in other Sarbecoviruses. A novel multibasic furin cleavage site (FCS) confers numerous pathogenetically advantageous capabilities, the existence of which is difficult to explain though natural evolution; SARS-CoV-2 to human ACE2 binding is far stronger than SARS-CoV, yet there is no indication of amount of evolutionary adaptation that SARS-CoV or MERS-CoV underwent. The flat topography of the ganglioside-binding domain (GBD) in the N-terminal domain (NTD) of SARS-CoV-2 does not conform with typical host evasion evolutionary measures exhibited by other human coronaviruses. The combination of binding strength, human and mouse peptide mimicry, as well as high adaptation for human infection and transmission from the earliest strains might suggest the use of humanized mice for the development of SARS-CoV-2 in a laboratory environment. The application of mouse strains expressing human ACE2 for SARS-CoV-related research is well documented (Ren et al. 2008; Hou et al. 2010; Menachery et al. 2015; Cockrell et al. 2018; Jiang et al. 2020). Additionally, culturing and adapting coronaviruses to different cell lines, including human airway epithelial cells, has been experimentally conducted in various laboratories (Tse et al. 2014; Menachery et al. 2015; Zeng et al. 2016; Jiang et al. 2020). While a natural origin is still possible and the search for a potential host in nature should continue, the amount of peculiar genetic features identified in SARS-CoV-2′s genome does not rule out a possible gain-of-function origin, which should be therefore discussed in an open scientific debate.