Covid-19 News

  • Personal comments.


    I've exercised some restraint on this thread but being continually called a troll, a paid fudder, an "entity", even a "middle manager" (whatever that is, but sounds pretty loathsome) is trying even my long patience. Nothing could be further from the truth, and many people here know it.


    Mods please stop it, or I will feel justified in replying to any future such with an accurate estimate of offending poster's characteristics, in a way not calculated to reduce tensions.


    Maybe some here might take my ignoring such comments, repeated again and again with impunity, as evidence that they are in fact true? Well, if so, I'd better stop ignoring them!

    • Official Post

    Personal comments.


    I've exercised some restraint on this thread but being continually called a troll, a paid fudder, an "entity", even a "middle manager" (whatever that is, but sounds pretty loathsome) is trying even my long patience. Nothing could be further from the truth, and many people here know it.


    Please comply with this request. you know that this place is an 'orderly house'.

  • Nobody denies that mutations do happen naturally! But if they do happen then you should also see the intermediate steps - not all, but at least a few. If you don't see the intermediates then these mutations are lethal and the chain does stop. A good rule of estimate is that 1 out of 10 is a good mutation = enhanced fitness and 1 out of 10 is neutral. In average 8 mutations are lethal.

    The average virus mutation rate is 1 a week. This means one acid changes what is tiny change only. Now we have a best match of 93%. A corona virus has about 30'000 base pairs https://books.google.ch/books?…22viral%20size%22&f=false thus 3% is 900 changes what takes 20 years if all changes just by luck happen at the expected places and are positive ones.


    Best match to SARS-CoV2 in bats found so far is 96% not 93% RTAG13 https://www.nature.com/articles/d41586-020-01449-8


    But there is a 93% match virus that proves an important point about viability of polybase insertion in Furin cleavage point, which is what W misunderstood I believe.


    Educating wyttenbach (does it work? Can it work? watch here for the next exciting installment).


    So what is the difference between:

    • point mutation?
    • insertion?
    • recombination?


    each is a single step change, but can result in 50% change in genetic material.


    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7106159/

    Recombination is a pervasive process generating diversity in most viruses. It joins variants that arise independently within the same molecule, creating new opportunities for viruses to overcome selective pressures and to adapt to new environments and hosts. Consequently, the analysis of viral recombination attracts the interest of clinicians, epidemiologists, molecular biologists and evolutionary biologists. In this review we present an overview of three major areas related to viral recombination: (i) the molecular mechanisms that underlie recombination in model viruses, including DNA-viruses (Herpesvirus) and RNA-viruses (Human Influenza Virus and Human Immunodeficiency Virus), (ii) the analytical procedures to detect recombination in viral sequences and to determine the recombination breakpoints, along with the conceptual and methodological tools currently used and a brief overview of the impact of new sequencing technologies on the detection of recombination, and (iii) the major areas in the evolutionary analysis of viral populations on which recombination has an impact. These include the evaluation of selective pressures acting on viral populations, the application of evolutionary reconstructions in the characterization of centralized genes for vaccine design, and the evaluation of linkage disequilibrium and population structure.


    https://www.nature.com/articles/d41586-020-01449-8

    It’s useful to know which animals are susceptible, to manage the risk that they might become virus reservoirs and possible sources of infection in people, says Michelle Baker, a comparative immunologist at the Commonwealth Scientific and Industrial Research Organisation in Geelong, Australia. But when trying to narrow down the culprit, it seems sensible to focus on those animals in close contact with bats, she says.

    Animals at wildlife farms in China are one of the first places to look, says Peter Daszak, president of the non-profit EcoHealth Alliance in New York City. Farms stock many captive-bred animals, from civets to raccoon dogs and coypu, a large rodent, often living close to livestock such as pigs, chickens and ducks. “These farms are usually wide open to bats, which feed at night above the pens, and some of which roost in the buildings. They are also usually linked to people’s houses so that whole families are potentially exposed,” says Daszak, who has visited many villages, wildlife markets, bat caves and farms in southern China over the past 15 years.

    “The opportunities for these viruses to spill over across a very active wildlife–livestock–human interface is clear and obvious,” he says.



    New viruses, or zoonotic jumps, are typically made by one-off unlikely jumps where a virus change (maybe a recombination with some other virus) alters fitness, or sometime direct from an animal surviving virus that can also adapt to humans. Once virus can replicate in host other changes are then possible optimising the viral genome locally for its host, which also usually means making it less deadly.


    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7248068/

    Mutation and adaptation have driven the co-evolution of coronaviruses (CoVs) and their hosts, including human beings, for thousands of years. Before 2003, two human CoVs (HCoVs) were known to cause mild illness, such as common cold. The outbreaks of severe acute respiratory syndrome (SARS) and the Middle East respiratory syndrome (MERS) have flipped the coin to reveal how devastating and life-threatening an HCoV infection could be. The emergence of SARS-CoV-2 in central China at the end of 2019 has thrusted CoVs into the spotlight again and surprised us with its high transmissibility but reduced pathogenicity compared to its sister SARS-CoV. HCoV infection is a zoonosis and understanding the zoonotic origins of HCoVs would serve us well. Most HCoVs originated from bats where they are non-pathogenic. The intermediate reservoir hosts of some HCoVs are also known. Identifying the animal hosts has direct implications in the prevention of human diseases. Investigating CoV-host interactions in animals might also derive important insight on CoV pathogenesis in humans. In this review, we present an overview of the existing knowledge about the seven HCoVs, with a focus on the history of their discovery as well as their zoonotic origins and interspecies transmission. Importantly, we compare and contrast the different HCoVs from a perspective of virus evolution and genome recombination. The current CoV disease 2019 (COVID-19) epidemic is discussed in this context. In addition, the requirements for successful host switches and the implications of virus evolution on disease severity are also highlighted.

  • The control class looks to be have misjudged their ability to pull this off. Aluminum cannot penetrate through thick steel columns. But the inherent fear of "the other" and the clash of civilization narrative was effective. It was a Hollywood film and we paid trillions in tickets willingly. And this film is bold, but I think it will be harder to suppress the science and I don't think we want to pay anymore.


    "They" must be paying heavily to pull in favors from all angles. Now the top journals in the field are compromised and in a wretched position, like Science and NEJM.


    In a stunning moment the former French Health Minister has given us the goods. We knew the science, but now we know they know that we know they are criminals against humanity. If you don't speak French turn on the text CC.


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  • Wyttenbach: To improve your troll rating [referring to THH]


    That is enough, thrice warned - or whatever they say.


    I am not a troll, but you, on this thread, argue in a way that is a unscientific, a disgrace, and creates much noise with little enlightenment. You latch onto certain memes and quote them as though they answer all questions - while ignoring all other questions.


    I would enjoy debating these issues with someone capable of having reasoned debate. That means listening accurately to the opposite points and critiquing them. It means responding directly to critiques. It means giving links to justify your assertions. None of this you do, not even a little bit. There are always alternate views. There is an argument for SARS-CoV2 being a lab-originated virus although there is no evidence for this, much against, and purely in terms of likelihood who would possibly want to engineer such a thing? Respiratory pandemics know no borders and are of use to no-one.


    On your specific argument about mutation, that leaves out the (likelihood) of a recombination occurring matching a human-compatible RBD (whether from Pangolins or somewhere else) with bat beta-CV rest. That could be via some intermediate not yet found (they are not easy to find) in some other species in that zoonotic disease dream - the Wuhan live market. All the elements have been found in nature. the mechanism for combining them (recombination) is well known and clearly not done via point mutation steps as you erroneously and naively argue.


    Over your absurd 3% 4% 6% argument, it helps to pay attention. If you knew the closest match was 97% (sounds like 96% rounded up to me) you could give the virus name, it would be interesting and we could all see whether it was the same as 96% RATG13 or not. In that case your argument about 93% was specious and silly - deliberately misleading. That is the trouble with your posts - they are detail-free. I can see this is necessary to you because you are make so many errors that fewer details allow you to gloss over things better: but i'd enjoy reading your stuff much more if i had the details justifying your sometimes interesting and usually distorted claims.


    May 13th and closest match quoted was still RATG13 (96.1%) so I doubt your 97% though it is certainly not impossible. Since RATG13 is not a direct ancestor we are still looking for a closer natural relative, but this is par for the course with these viruses - it is difficult to locate the exact crossover animal. What we can see is that it is very similar to stuff out there, and all the bits are plausibly there.


    I adopt the principle - which I'm sure many share, of not believing any argument put forward by anyone here. None of us are experts. That is why I give links, and that is why I find links from others (as long as not contrafactual Fox TV opinion) interesting. Actually I find contrafactual Fox TV interesting in an anthropological sense a well, but politics and social commentary about that is OT for this thread.


    I'd recommend to you less bluster and more hard fact contribution to this debate.

  • Even when angry, THH is unable to be unpolite. The stupid argument that he is a troll is somewhat caused by the fact that he feels the compulsive need to debunk every single idiocy written here, which requires such an exceptional patience that it ends up being suspect. And a huge workload!

  • RB - I try to give you credit for the ability to appraise other work.

    Here is my appraisal of Montagnier's..preprint... https://osf.io/tgw2d/ expressed in simple terms for the benefit of THH..


    No probability numbers.. Therefore I cannot compare with Etienne's " absurd.".

    Probability is the heart of the matter... and not irrelevant as THH appears to maintain.


    Its really up to Etienne and Montagnier to come up with probability numbers which fund their "most likely" and "adsurd"

    or perhaps THH our new forum expert on viral genetics..can come up with some number

    Etienne .......may be able show that the mutation rates are ..95% ..probable based on random mutation

    Montagnier may be able show that the mutation rates are ..5% probable based on random mutation


    on the other hand they may not be able to show this at all..

    because of the number of variables involved...

    In that case ... there is ample space for wordy dialectic and endless fruitless conjecture..until this thread ends


    I expect with 99 % probabilty that THH will ONLY be able to show his wordy evolutionary wandering dialectic..

    based on the fact that this is ALL he could show in the face of four simple spreadsheet columns of calorimetry data.

    with far less variables.. Clearance Items

    Montagnier/Perez

    ..HIV1, HIV2 and SIV retroviruses most likely are present into the genome of COVID19

    An analysis of amino acid homologies confirms the very probable insertion of this EIE in COVID_19,

    It is very likely that there was HUMAN INTERVENTION in this LYONS's region


    Étienne Simon-Lorière

    "If we take a word from a book and that word resembles that of another book, can we say that one has copied from the other?”Its's absurd

    https://www.lepoint.fr/sante/e…17-04-2020-2371881_40.php

  • Étienne Simon-Lorière


    "If we take a word from a book and that word resembles that of another book, can we say that one has copied from the other?”


    No - we cannot.


    Much more likely (think all those middle ages texts) that stories in different books are related and have a common ancester. Similarity is found everywhere, sometimes more directly copied but more usually as two branches on a tree.


    This is a pretty exact analogy for genetic evolution. We even have recombination - a book that contains stories from different halves of two other books. Though here the analogy breaks down a little because there is less similarlity between differnet stories than there is between different coronaviruses, all of which need more or less the same molecular machinery, with some variants for each functional component.


    LOL


    I guess as far as experts go the links (RB - you should always give them, then we can see the paper and look for academic comment on it from others) earlier showed pretty conclusively that this guy is has way out opinions, refuted by pretty well everyone else.


    So if you follow his ideas of probability you will end up with very unusual notions of what is likely!

  • THHuxleynew


    It is up to you to show a possible evolution path from any possible source virus to CoV-19. As long as you cannot do it your hypothesis is just a dream. Writing down the few lab steps do to it with Crisper-Cas on the other side is easy. Needless to repeat that the Swiss army lab already 3 months ago did a full bottom up syntheses of the whole Cov-19 virus.


    What you possibly did overlook: The matching rates depend on what you try to achieve. Closest random match bet pattern match. Thus if you argue for recombination then I in your place would check for the best matching pattern virus not for the best random match.


    Is that already to much?


  • I fail to see the relevance of the fact that labs can synthesise a virus with a known genome? Surely that is general (non-expert) knowledge and says nothing about origins, since it applies to all viruses?


    W: were you an expert on these issues I would still look to other experts to check - since even experts - on any issue - can have varying opinions.


    But you are not an expert, and give no credible linked support from experts to your comments, so I'm not going to do anything.

  • The stupid argument that he is a troll is somewhat caused by the fact that he feels the compulsive need to debunk every single idiocy written here, which requires such an exceptional patience that it ends up being suspect.

    mea culpa. But I sort of enjoy it, and do it v quickly hence mistakes from time to time.


    Partly, with COVID, as with many new things, I really enjoy understanding what is going on - this place helps me do that.


    That does not make the misery of a totally and mostly unnecessarily wrecked UK any better though.

  • Avigan

    Dr. Peter Michalos: Avigan 'Quite Amazing' in Reducing COVID-19 Recovery Time

    https://www.newsmax.com/us/pet…ent/2020/06/14/id/972102/


    Avigan, is being tested in Massachusetts and is "showing exciting" results and might be available …...

    Avigan has shown in trials of treating COVID-19 to cut the recovery time down from 11 days to just five. It was developed in Japan many years ago for the flu and repurposed for Ebola a few years ago......

    "Avigan is looking quite amazing," he added, noting use of treatments like hydroxychloroquine and remdesivir has to come early as opposed to later, when the virus takes over the lungs and leads to the immune system destroying a patient from within.

    "The trick with a lot of these medicines is early intervention so the virus does not replicate," Dr. Michalos concluded. "The problem is once it replicated and gets into the lungs and our immune system starts filling it up with fluid."

  • Avigan, is being tested in Massachusetts and is "showing exciting" results

    Hopefully Avigan works... one good thing is that a cheap generic version is being manufactured now.. with aid of Russian capital


    In Japan PM Abe appears to be frustrated with the progess of Avigan


    TOKYO -- When Prime Minister Shinzo Abe learned that the Avigan flu medicine would not be approved for the coronavirus by the end of May, he was furious. "That's not what I was told," he lashed out at aides.

    https://asia.nikkei.com/Politi…ed-way-for-Avigan-blunder

    however in Russia the approval process has been more rapid..less checks and balances there,, but then there are more deaths ihan in Japan


    "Russia’s health ministry recently approved a new anti-viral drug for COVID-19 called Avifavir

    https://www.trialsitenews.com/…s-to-supply-saudi-arabia/

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