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    Covid-19: Is Herd Immunity Possible At This Point?

    Former covid patients appear to be losing their antibodies quickly
    by Adam Taggart

    Friday, July 3, 2020, 8:00 AM

With total covid-19 cases worldwide having punched above 10 million and the US now experiencing 50,000(!) new infections per day, the end to the pandemic looks nowhere in sight.

For those hoping a vaccine will ride to our rescue, we’re stuck in a cycle of good news/bad news as nearly every promising initial announcement is soon followed by a list of setbacks. Complicating the matter is that former covid patients appear to be losing their antibodies quickly — suggesting that lasting immunity may not be a realistic expectation.

Meanwhile, more research data is pointing to the conclusion that the virus did develop, in part, in a lab. With 90% confidence.

Oh boy…

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85 Comments

  • Fri, Jul 03, 2020 - 9:00am

    #1
    nelson47@protonmail.com

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    Oh Boy is Right,

     Just what I need in my immune system. Can't wait for to add mercury to my blood stream.

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  • Fri, Jul 03, 2020 - 9:45am

    #2

    thc0655

    Status: Platinum Member

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    1,000 Chihuahuas?!

    A thousand Chihuahuas glomping onto you while you’re running across a field?

    I’m going to have Chihuahua nightmares tonight!

    Would you really want Jacinda Arden to be your President? You would have to turn in most of your guns, and ALL of the ones most useful in a civil war or mass civil unrest.

    I enjoy listening to you criticize the incompetence, greed and politicization of science and medicine. Or more to the point: the incompetence, greed and politicization of scientists and physicians (“they have names”). Listening to you I’ve started to get the impression that science and medicine are as screwed up as law enforcement (not to mention banking, government, corporations and “”markets””). Since the experts in science and medicine who are failing us are much, much more intelligent than the average cop, I’m guessing a lot of them qualify as “the dumbest smart person I’ve ever met.”

    But where are the mobs rioting while screaming “Ban gain of function research!” “Defund Science!” “Defund Medicine!”

    You often quote Charlie Munger saying, “Show me the incentive, and I’ll show you the outcome.” So I’m looking forward to your ideas on how to drastically reform the incentives for scientists and doctors like you did for law enforcement. Or maybe you’d rather I do it.

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  • Fri, Jul 03, 2020 - 9:55am

    #3
    ronaldmignery

    ronaldmignery

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    Herd immunity already?

    If antibody levels can decline to undetectable in as little as two weeks after infection yet resistance remains from T-cells, is it not possible that  herd immunity already exists in some parts of the word and the USA?  Specifically, NY, NJ, MA, RI, and CT, unlike other states, all see no new rises in cases in spite of demonstrations, openings, etc.  What they have in common is deaths per million around 1000 or greater.  Since deaths/M is likely the most robust statistic for covid19, perhaps one could say that herd immunity arrives when the fatality rate reaches 0.1% (maybe lower as treatment methods improve).

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  • Fri, Jul 03, 2020 - 10:10am

    #4
    Ision

    Ision

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    Why Does It Take Months For People To Get a Clue...

    The first time I saw the genome of this virus, I knew a vaccine could not be created for it...I knew there would be no such thing as "herd immunity" against it...I knew it was a laboratory creation....I knew from the disinformation being spewed the virus was deliberately released...and told everyone about it.

    I tried to inform people this virus would mutate rapidly and that reinfection would be possible as a result; that people could be infected by more than one strain at the same time.

    I told people a cure would already exist, and already be on the shelf...while every effort to misdirect outside efforts to fight this virus was instigated to drive efforts along ineffective and meaningless goals.

    Why is all this still a surprise after all these months?

    When I was part of the Intelligence Community, and was specifically trained about such pathogens, such as what is now called, "HIV," for example,  and other bio-weapons, including how these pathogens are intended to be used (since it was part of my job to keep selected personnel alive), I have first hand knowledge...as I sat with others in government classrooms, in classified areas, and was instructed, in detail, about such viral pathogens.

    Short of an effort to avoid nuclear exchange, the only reason to release such pathogens are population control, and the achievement of a political objective, or both.

    I had thought there was a chance this pathogen was released accidentally, while the virus was just manifesting in China, but the Confusion Game became immediately obvious..and I now believe this is a "Plandemic" and not accidental.

    I wish everyone worthy of Life...Life.

     

     

     

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  • Fri, Jul 03, 2020 - 10:35am

    #5
    Prep101

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    Bill Gates & Vaccines links

    There is no way I will take a vaccine that is funded by Bill Gates. Unfortunately, his money is to be found pretty everywhere when it comes to vaccines. If you want to know why I am saying this, the documentary to which I link below is a MUST WATCH.

    Part One: How Bill Gates Monoplized Global Health

    Part Two: Bill Gates' Plan to Vaccinate the World

    Part Three: Bill Gates and the Population Control Grid

    Part Four: Meet Bill Gates

    I've linked to this documentary before, but I now link to it again, because I think it is THAT important. You can also read the Transcript, and check out all the sources and hyperlinks.

    https://www.corbettreport.com/gates/

     

    For even more context and background, I recommend you check out:

    https://www.corbettreport.com/bigoil/

     

    If you want another source than The Corbett Report on this topic (The Great Reset), I recommend Martin Armstrong:

    The Great Reset now Available for Download

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  • Fri, Jul 03, 2020 - 11:01am

    #6
    glixon66

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    My body, my choice chant

    How about “My Stupidity, My Choice”?

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  • Fri, Jul 03, 2020 - 11:26am

    Mohammed Mast

    Mohammed Mast

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    Hey THC

    Check it out. This is what defunding the police looks like.

    https://www.youtube.com/watch?v=wj1BKa79OiI

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  • Fri, Jul 03, 2020 - 12:13pm

    kunga

    kunga

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    Clueless

    Hi, Ision, good to hear from you.  It is hard for a rational voice like yours to cut through the confusion fog.  I hope when the US Constitution is rewritten, they remove that amendment of the right to breed and wreck the earth.

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  • Fri, Jul 03, 2020 - 1:01pm

    #9
    MQ

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    early chinese reports

    Weren't there reports of people in Wuhan who had the virus and kicked it on their own being reinfected later and becoming extremely ill or dying?

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  • Fri, Jul 03, 2020 - 1:07pm

    #10
    Bleep

    Bleep

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    Compilation of Mask Studies

    Has anyone compiled a list of scientific studies on mask efficacy? Also, what do people plan on feeding chickens if they can’t buy feed anymore?

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  • Fri, Jul 03, 2020 - 1:42pm

    kunga

    kunga

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    Chicken feed

    I don't have chickens, but have thought about the feed availability issue.  What I am researching is growing corn, sunflower seeds and meal worms.  All can be done low tech.

    Edit:  Also, earthworms.

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  • Fri, Jul 03, 2020 - 2:12pm

    ronaldmignery

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    ronaldmignery said:

    Klaatu: No - Not T-cells from other corona viruses but rather T-cells from covid19 left over after antibodies have diminished below detection thresholds, T-cells specific for covid19 that can resume an antibody response before covid19 can reinfect to the level where symptoms present.

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  • Fri, Jul 03, 2020 - 2:32pm

    #13
    jn20

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    jn20 said:

    Hi,

    I am new to this site, but regarding antibodies I want to point you to the informational video about the Danish antibody testing. It is developed by our health authorities, hospitals and our largest pharma company Novo Nordisk.

    Antibody testing:

    https://www.youtube.com/watch?v=SCvxrzSgyik

     

    PCR testing:

    https://www.youtube.com/watch?v=oCZ-wd67gzw

    Looking forward to more videos.

    Kind regards,

    Jeppe

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  • Fri, Jul 03, 2020 - 2:49pm

    David Kendrick

    David Kendrick

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    David Kendrick said:

    Or the population supplements - if they like it or not, e.g. Fortified cereals. BAME and poor diet seems to be the big risk factor.

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  • Fri, Jul 03, 2020 - 3:02pm

    David Kendrick

    David Kendrick

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    Defund the Police

    In the UK VAP crime rate rose from 1901 to 1998 7708% Rapes by 1743% Robbery 16783% most of which was from 1970, during which time the police were well funded and by and large stopped policing. They were in a time where unlimited EU and Asian immigration happened(so we got their criminals out to make something of themselves in a nation where they were not known), but they knew what was happening with their suspects and did and said nothing about it. If they were working farm animals, the farmer would have put them down. We can do better paying off a local don who would ensure unlicensed criminality would get the full force of injustice.

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  • Fri, Jul 03, 2020 - 4:23pm

    #16

    Oliveoilguy

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    Science Communicators like Chris are essential

    Special thanks to Chris for being a Science Communicator in a politicized environment that throws roadblocks against him at every turn.

    By virtue of what I am learning on Peak Prosperity, I am able to have some positive impact on my local community. So hats off to Chris and to other enlightened contributors on PP who struggle to discern and communicate the truth every day.

    “Science is but an image of the truth” Francis Bacon

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  • Fri, Jul 03, 2020 - 4:37pm

    #17
    kunga

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    Stupid is as ...

    My grandfather, who was a college professor probably would qualify as a "stupid smart person."  He died long before I was born, but I probably carry the taint, against which I do struggle when I remember.  He was well known for building a huge, beautiful farm house, before digging the well.  It was the view, I guess.

    That warning being given, my speculation, proved or not in some distant future, is, that antibody production depends on Vitamin D status.  Most of the "long haul" case reports never mention any supplements or immune boosting they were doing before infection.  This is partially the fault of our crappy medical system.  All my own opinion.

    Edit:  evidently, vitamin C plays a large role in level of antibodies in the serum.

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  • Fri, Jul 03, 2020 - 5:24pm

    #18

    Oliveoilguy

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    Lack of Antibodies

    So ...if there is minimal or no antibody buildup, the only herd immunity can be from the members of the herd that are immune by virtue of their own chemistry before, during and after they are exposed to Covid. The only thing that changes the Math is the death of part of the population. The immune part of the population in the equation is a constant.

    That brings us back to prophylaxis. A healthy lifestyle and the correct supplements. And a plan B to get some HCQ if you can ......and be an advocate for the New studies that show HCQ positive so that the public will wake up and be as vocal as the conspirators.

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  • Fri, Jul 03, 2020 - 7:00pm

    Christina Watkins

    Christina Watkins

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    Christina Watkins said:

    Ision very interested to read more of your posts. However, when I tried to search by username your posts don't show up? I believe your most recent post is spot on. Am interested to read more.

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  • Fri, Jul 03, 2020 - 9:43pm

    #20
    Island girl

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    The batwoman from WIV was also researching antibody dependent enhancement mechanisms in 2019

    Dr. Shi Zheng Li was coauthor on a research into how corona viruses can infect antibody producing cells when antibodies attach themselves to the spike protein. The research was done with MERS coronavirus in the context of mechanisms of antibody dependent enhancement.

    https://jvi.asm.org/content/94/5/e02015-19#sec-6

    Here we identify a novel mechanism for ADE: a neutralizing antibody binds to the surface spike protein of coronaviruses like a viral receptor, triggers a conformational change of the spike, and mediates viral entry into IgG Fc receptor-expressing cell.

    I'm no expert in immunology, but I wonder about pertinence to SARS Cov-2, perhaps the attenuation of acquired immunity, and the consequences of later reinfection. I recall reading that some people seems to get coronavirus more than once and worse symptoms the second go-round. I wonder about relevance to vaccines.

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  • Fri, Jul 03, 2020 - 10:27pm

    Pappy

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    Chicken feed options...

    It's all about the grubs, grains, bugs and worms.  If you have the space, keep a couple patches of earth tilled, rotating every week between the two.

    The chickens will find their own food in the soil.  Friend of mine had chickens on his farm and he only fed them in the winter here in Wisconsin.  And they thrived on bugs, native grains, grubs and worms from his fields.

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  • Fri, Jul 03, 2020 - 10:41pm

    #22

    sofistek

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    Now, the evidence is clearly in favour of masks

    Just spotted this article about why people should wear masks (even if no-one else does).

    https://www.ucsf.edu/news/2020/06/417906/still-confused-about-masks-heres-science-behind-how-face-masks-prevent

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  • Sat, Jul 04, 2020 - 3:14am

    Mpup

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    Another great find Island Girl, you go girl.

    Notice the funding for this study was provided by:  The National Institute of Allergy and Infectious Diseases,  of whom Dr. Anthony Fauci is the director.   If he would lie to us about the wearing of masks EVERYTHING that comes from him is suspect.  While it appears this study was well intentioned:  "This study reveals complex roles of antibodies in viral entry and can guide future vaccine design and antibody-based drug therapy."  the date of submission was November 27, 2019.  The Chinese government and WHO state the first confirmed case of Covid-19 was December 8, 2019.   A study gone bad?

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  • Sat, Jul 04, 2020 - 9:50am

    #24
    socaljoe

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    socaljoe said:

    "...the US now experiencing 50,000(!) new infections per day"

    Chris, you are confusing "cases" and "infections". I suspect "new infections" have been 50,000 per day for a long time... likely much, much higher. We are finally seeing them as "new cases" since we are testing much more. There are so many asymptomatic or mild infections, I would be willing to bet that new infections are several times greater than new cases.

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  • Sat, Jul 04, 2020 - 6:46pm

    #25
    Island girl

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    Herd immunity and T Cell responses - two recent studies

    The Swedes have a new study on T-cell immunity that they find encouraging. They seem to think it is protective  but not sure how much when patients don't also mount antibodies

    Here's their press release:

    https://news.ki.se/immunity-to-covid-19-is-probably-higher-than-tests-have-shown

    Here is the preprint:

    https://www.biorxiv.org/content/10.1101/2020.06.29.174888v1

    And an interview quote:

    "Our results indicate that roughly twice as many people have developed T-cell immunity compared with those who we can detect antibodies in," noted Karolinska Center for Infectious Medicine researcher Marcus Buggert...."It remains to be determined if a robust memory T cell response in the absence of detectable circulating antibodies can protect against [the virus]."

    The Germans have also published a study in T-cells. My immunology knowledge is not good enough to comment on it.

    https://www.researchsquare.com/article/rs-35331/v1

    But there is a news report about it - claims the implication is that having had the common cold may confer some immunity (T-cells have some memory). I wonder what that means for those who get regular flu shots?

    https://www.sciencetimes.com/articles/26278/20200630/8-out-10-people-infected-covid-19-protected-episodes-colds.htm

     

     

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  • Sat, Jul 04, 2020 - 7:22pm

    #26
    Island girl

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    T cell immunity as discussed in German study

    As I noted, not an immunologist, but I did peruse the German paper referenced above paper and was intrigued by this discussion point:

    "recognition rates of SARS-CoV-2 T-cell epitopes by individual donors were lower in individuals with more severe COVID-19 symptoms. This observation, ... and reports from other active or chronic viral infections associating diversity of T-cell response with anti- viral defense, provide evidence that natural development and vaccine-based induction of immunity to SARS-CoV-2 requires recognition of multiple SARS-CoV-2 epitopes.

    Translation: I think it means that your immune system needs to recognize more than a single local region of the viral antigen(s) in order to mount a robust response.

    If that is the case, I wonder what this means for the Moderna mRNA vaccine. According to their website, they pre-select the protein they will use as antigen and synthesize the mRNA for it.

    I wonder what guides the selection of the antigenic protein in the case of SARS Cov-2. (I am aguessing the spike protein is a likely candidate , but that's speculation on my part). DO we know which viral proteins would provide the "multiple epitopes" necessary to mount a robust response, or are we guessing?

    A theory is only as good as the assumptions on which it is based. I hope the Task Force is looking at the data coming in from beyond our shores.

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  • Sat, Jul 04, 2020 - 8:01pm

    Island girl

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    Replying to Mpup

    Yes, the timing of study is interesting (FYI - she reports on MERS but no doubt work on SARS was in the mix). By 2015 they had already created their chimeric Frankenvirus (my words, not theirs) with the increased infectivity, lung cell pathogenicity and muted neutralization by antibodies, as cited in an earlier post. So by 2019, antibody dependent enhancement research seems to have been underway, and I suspect if it weren't for the emergence of SARS Cov 2 we would have seen more reports.

    As to funding, yes, isn't it ironic. I suspect you are aware that the funding for GOF was paused in 2014 (the 2015 GOF research got published though) and then resumed in 2019, because, well...what could possibly go wrong?

    I cite from the NIH website:

    "The U.S. government will undertake a deliberative process to assess the risks and benefits of certain gain-of-function (GOF) experiments with influenza, SARS, and MERS viruses in order to develop a new Federal policy regarding the funding of this research. During this deliberative process, U.S. government agencies will institute a pause on the funding of any new studies involving these experiments. For purposes of the deliberative process and this funding pause, “GOF studies” refers to scientific research that increases the ability of any of these infectious agents to cause disease by enhancing its pathogenicity or by increasing its transmissibility among mammals by respiratory droplets.

     

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  • Sat, Jul 04, 2020 - 8:07pm

    #28
    tbp

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    Chris Martenson not asking the basic questions?

    Why did he fail to ask one of the most important questions: Will this experimental covid vaccine come filled with aluminum and other neurotoxins that previous vaccines are all laced with?

    You say you want the "terrain to be as fit as it can be"... but you say nothing about the typical vaccine adjuvants obliterating the terrain...

    That research you should've done even before considering the shady (to say the least) characters leading the efforts to suppress effective cures (like HCQ) to get to mass vaccination programs, as Prep101 points out.

    If you inject aluminum into a child without a developed blood-brain barrier (BBB), what should you expect to happen? Watch Vax xed II: The People's Truth (2019) if you're ready to face the obvious truth of the predictable effects of vaccine adjuvants (which are often primary ingredients, the attenuated pathogen a secondary ingredient if ranked by effects of the substances injected). [Oh wait, I can't post bitchute links, nope, those remain BANNED on PeakProsperity! - You'll have to paste the link together or search for it: bit chute .com/video/ 1RAAGIgNLeJU/ ]

    How much longer do you intend on shying away from the truth about vaccines[-as-they-are-today]?

    The biggest risk factors for Covid seem to be:

    1) Vitamin D deficiency (aggravated by lockdowns but lessened by summer time)
    2) Vaccine toxins exposure (elderly populations being injected with flu shots containing several extremely toxic adjuvants, maybe even containing other coronavirii and XMRVs)

    This is because, prior to the coronavirus pandemic, there has been and is a vitamin D deficiency pandemic, and a vaccine injury pandemic.

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  • Sun, Jul 05, 2020 - 12:58am

    Mpup

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    Reply to IG :)

    "Chimeric Frankenvirus" indeed.    Your comments as well as others here are some of the most salient anywhere.  We (governments, power brokers, and much of the scientific/medical field) seem to be in a CYA, tow the line, propagandist mode.  It's  as though we're in a "you want the truth? you can't handle the truth" period.  In the interim, tens of thousands continue to die.   Throughout history, science has been a search and quest for the "truth".   Sadly today, "truth" has become obfuscated to irrelevance, bought with the dollar, and the majority of the masses cheering it's demise.

    If (and it appears it was) this virus was created through gain of function studies, let us hope and pray it's makers haven't created the perfect monster.  I pray all here know the peace, patience, and understanding, needed in these difficult times.  The "Truth" will set us free.

    edit to remove language in poor taste.

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  • Sun, Jul 05, 2020 - 8:11am

    #30
    Steve

    Steve

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    Which video?

    Does anybody know which video it was where Chris presented a protocol from a US medical college that corroborated his protocol for boosting the bodies immune system?  ... vit C, Quercetin, Vit. D3, Vit C, Selenium...

    If so, please share the video.

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  • Sun, Jul 05, 2020 - 11:05am

    #31
    perspective001

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    Not 'Just Another Flu'

    Leaving aside, for now, both the idiotic government (all governments) response to this bio weapon and the myriad ways 'deaths' are being counted, the death metric is not capturing the true cost of this virus. Many more people who get the virus and do not die do get maimed for life. Decreased lung and other organ function, nerve damage that can leave a person in various levels of pain plus reinfection which makes damage cumulative with each bout. This is not a 'just another flu' virus. It is a bio weapon and the hobbling wounded are going to start to matter as the infection count goes up.

    Government is not going to protect you. You need to protect you. Because you are going to have to live with the decisions you make.

    Stanford Doc: COVID Fatality Rate For People Under 45 Is "Almost 0%" | Zero Hedge
    https://www.zerohedge.com/political/stanford-doc-covid-fatality-rate-people-under-45-almost-0

    Stanford Doc: COVID Fatality Rate For People Under 45 Is "Almost 0%"

    ...for 45 to 70, it is probably about 0.05%-0.3%. For those above 70, it escalates substantially...

    www.zerohedge.com

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  • Sun, Jul 05, 2020 - 3:01pm

    #32
    jn20

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    Self-replicating mRNA vaccine

    Interestingly enough, one can make a self-replicating mRNA vaccine. Take the genes (structure of active polymerase solved and published in nature) for the viral RNA polymerase put it on a mRNA also containing the viral spike protein. Then use lipofection to get cells to take up the vaccine. Et voila, the infected cells start producing viral RNA polymerase, which synthesise additional mRNA. Spike protein will be produced and delivered to the cell surface, while viral polymerase fragments can get presented by MHC proteins on the cell surface, inducing both B and T cell responses respectively.

    And yes, I did preliminary design on such a vaccine and came up with a way to test it in cell cultures and animal models.

    Kind regards,

    Jeppe

    EDIT: The vaccine cannot produce infectious virus particles as no structural proteins are present.

    EDIT EDIT: Here is an overview of the status of some of the vaccines being developed:Vaccinestudier - Overblik over planlagte og igangværende humane studier af vacciner til COVID-19

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  • Sun, Jul 05, 2020 - 8:03pm

    Island girl

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    The virus might down-regulate of MHC expression. Woudl that affect this apporach to a vaccine?

    Replying to post 32. You seem to understand the immunology. Help me out here.

    I've been looking at research on the immune response to SARS Cov-2.

    A group in China is suggesting that an open reading frame on the SARS Cov-2 genome (ORF-8) enables this virus to evade immune surveillance by down-regulating the surface expression of MHC-1.

    https://www.biorxiv.org/content/10.1101/2020.05.24.111823v1.full

    This paper is disturbing because they point out that this open reading frame is the least homologous to analogous gene sequences in original SARS Cov, another strange way that this version 2 virus seems particularly adapted to be virulent.

    Question: if the mRNA vaccine primes the T-cells ahead of viral exposure, might that prevent  down-regulation of MHC-1 with subsequent exposure to the actual virus? Or would the actual virus still be able to evade eliciting a T-cell response via the mechanism in this paper?

    On the other hand, In a previous post, I shared a study by German scientists, which suggests that prior exposure to other coronaviruses may be somewhat protective via a T-cell pathway, although antibody titres may be low.

    So I'm not sure how to tie these different strands together.

    Also, do you think the Spike protein is the best candidate antigen for an mRNA vaccine? Is that what Moderna is using?

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  • Mon, Jul 06, 2020 - 9:27am

    #34
    tbp

    tbp

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    tbp said:

    @jn20
    Interestingly enough, one can make a self-replicating mRNA vaccine. Take the genes (structure of active polymerase solved and published in nature) for the viral RNA polymerase put it on a mRNA also containing the viral spike protein. Then use lipofection to get cells to take up the vaccine. Et voila, the infected cells start producing viral RNA polymerase, which synthesise additional mRNA. Spike protein will be produced and delivered to the cell surface, while viral polymerase fragments can get presented by MHC proteins on the cell surface, inducing both B and T cell responses respectively.

    Sounds great, but do you have any reason to believe it won't end up being laced with aluminum, polysorbate 80, formaldehyde, MSG, aborted human fetal tissue, animal organ tissue containing viruses... and other neuro-, immuno-, and cytotoxic adjuvants that seem to be the primary cause of the autism epidemic and a vast array of other health disasters?

    I don't disagree with talking about theoretical vaccines, but we can't just keep ignoring the health-destroying (and society-destroying as children are the main targets) adjuvants, which have literally turned vaccines into bioweapons, thinly veiled as medical necessities.

    @Island girl
    Also, do you think the Spike protein is the best candidate antigen for an mRNA vaccine? Is that what Moderna is using?

    That would seem to make the most sense, as without functional spike proteins, the virus would be inert (non-pathogenic).

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  • Mon, Jul 06, 2020 - 10:29am

    #35

    Oliveoilguy

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    Texas Doctor Richard Bartlett pitches” Budesonide” as Covid Cure

     

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  • Mon, Jul 06, 2020 - 12:10pm

    Rector

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    I guess our superiors will suppress this

    Can't have any independent thinking.  Must suppress.  How long till this is banned by Twit, FB, YT?

    Rector

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  • Mon, Jul 06, 2020 - 1:03pm

    #37
    Mohammed Mast

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    Video

    I posted this on the forum page.

    Watched the video. He made some claims about Taiwan, Singapore and Japan that I have not been able to verify.

    I hope it works but he was a little too evangelical and did not really present data.

    Need more info from other sources.

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  • Mon, Jul 06, 2020 - 1:12pm

    #38

    Jim H

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    This is super interesting Olive Oil.. Thank you!

    This new treatment could literally be the final nail in the coffin of the weaponized virus.

    Based on Doctor Bartlett's comments about other countries like Japan, Singapore, and Taiwan which have super low death rates, I did some digging.  I personally find it hard to believe that the mode of efficacy is just related to an immuno-modulation/anti-inflammatory effect.. could it be that simple?

    First off, we should say that one reason to think it does work is that WHO said not to use steroids.   Out of Japan in April;

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7161498/
    Therapeutic potential of ciclesonide inhalation for COVID-19 pneumonia: Report of three cases

    Abstract

    No specific and effective anti-viral treatment has been approved for COVID-19 so far. Systemic corticosteroid has been sometimes administered to severe infectious diseases combined with the specific treatment. However, as lack of the specific anti-SARS-CoV-2 drug, systemic steroid treatment has not been recommended for COVID-19. We report here three cases of the COVID-19 pneumonia successfully treated with ciclesonide inhalation. Rationale of the treatment is to mitigate the local inflammation with inhaled steroid that stays in the lung and to inhibit proliferation of the virus by antiviral activity. Larger and further studies are warranted to confirm the result of these cases.....

    ....Although it was still very preliminary and unpublished data, the coronavirus laboratory at the National Institute of Infectious Diseases, Murayama Branch, had experimental data that among existing inhalation drugs for treatment of bronchial asthma, ciclesonide (trade name: Alvesco) has strong antiviral activity against SARS-CoV-2 [1]. In addition, according to another screening studies including FDA-approved drugs, ciclesonide also has the antiviral activity against MERS virus [2].

    More going on than meets the eye?  I will dig more.

     

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  • Mon, Jul 06, 2020 - 1:18pm

    #39

    Jim H

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    Following the reference from the last paper.. here it is! In-vitro anti-viral activity of ciclesonide established

    This appears to be one of the inhaled corticosteroids that Japan is using for Covid-19.  Does Budesonide have similar properties?

    https://www.biorxiv.org/content/10.1101/2020.03.11.987016v1

    The inhaled corticosteroid ciclesonide blocks coronavirus RNA replication by targeting viral NSP15

    Steroid compounds, which are expected to have dual functions in blocking host inflammation and MERS-CoV replication, were screened from a chemical library. Within this library, ciclesonide, an inhaled corticosteroid, suppressed human coronavirus replication in cultured cells, but did not suppress replication of respiratory syncytial virus or influenza virus. The effective concentration of ciclesonide to block SARS-CoV-2 (the cause of COVID-19) replication (EC90) was 6.3 μM. After the eleventh consecutive MERS-CoV passage in the presence of ciclesonide, a resistant mutation was generated, which resulted in an amino acid substitution (A25V) in nonstructural protein (NSP) 15, as identified using reverse genetics. A recombinant virus with the mutation was also resistant to ciclesonide suppression of viral replication. These observations suggest that the effect of ciclesonide was specific to coronavirus, suggesting this is a candidate drug for treatment of patients suffering MERS or COVID-19.

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  • Mon, Jul 06, 2020 - 1:35pm

    #40

    Jim H

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    More data regarding ciclesonide as an anti-viral

    https://www.technologynetworks.com/drug-discovery/news/drug-screen-identifies-niclosamide-and-ciclesonide-as-antiviral-candidates-against-sars-cov-2-334337

    Korean researchers have screened 48 FDA-approved drugs against SARS-CoV-2, and found that 2, which are already FDA-approved for other illnesses, seem promising. The FDA approval for other uses would greatly reduce the time needed to gain FDA approval of use in COVID-19. The research is published in Antimicrobial Agents and Chemotherapy, a journal of the American Society for Microbiology.

    The investigators tested the drugs in Vero cells, a cell line developed from kidney cells of the African Green Monkey, which are commonly used to grow viruses for vaccine production.

    An anti-helminthic drug called niclosamide demonstrated “very potent” antiviral activity against SARS-CoV-2, according to coauthors Sangeun Jeon, Meehyun Ko, and their collaborators, of the Zoonotic Virus Laboratory, Institut Pasteur Korea, Seongnam, Korea. “Not surprisingly, its broad-spectrum antiviral effect has been well documented in the literature, including antiviral properties against SARS- and MERS-CoV,” they write.

    A downside of niclosamide is low absorption, which undercuts the drug’s power by reducing the dose that reaches the target tissue. However, “Further development or drug formulation could enable effective delivery of this drug to the target tissue,” according to the report.

    Despite substantially lower antiviral potency, ciclesonide, an inhaled corticosteroid used to treat asthma and allergic rhinitis, also showed promise against SARS-CoV-2. Intriguingly, the investigators note that a study published earlier this year ( by Matsuyama et al.) a treatment report of 3 patients infected by SARS-CoV-2, demonstrated antiviral activity and revealed the drug’s molecular target to be a viral protein called Nsp15.

    “With its proven anti-inflammatory activity, ciclesonide may represent as a potent drug which can manifest [the] dual roles [of antiviral and anti-inflammatory] for the control of SARS-CoV-2 infection,” the investigators conclude. The anti-inflammatory activity might play a critical role in dampening or preventing the cytokine storms, an immune inflammatory overreaction that can kill COVID-19 patients.

    Reference: Jeon, et al. (2020) Identification of antiviral drug candidates against SARS-CoV-2 from FDA-approved drugs. Antimicrobial Agents and Chemotherapy,  DOI: 10.1128/AAC.00819-20

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  • Mon, Jul 06, 2020 - 1:42pm

    #41

    Jim H

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    Boom: "Antiviral and Anti-Inflammatory Activity of Budesonide" paper from 2018

    Note:  The cold virus is a coronavirus.

    https://pubmed.ncbi.nlm.nih.gov/29407486/

    Abstract

    Human rhinovirus (HRV) infection causes more than 80% of all common colds and is associated with severe complications in patients with asthma and chronic obstructive pulmonary disease. To identify antiviral drug against HRV infection, we screened 800 FDA-approved drugs and found budesonide as one of the possible drug candidates. Budesonide is a corticosteroid, which is commonly used to prevent exacerbation of asthma and symptoms of common cold. Budesonide specifically protects host cells from cytotoxicity following HRV infection, which depend on the expression of glucocorticoid receptor. Intranasal administration of budesonide lowered the pulmonary HRV load and the levels of IL-1β cytokine leading to decreased lung inflammation. Budesonide regulates IL-1β production following HRV infection independent of inflammasome activation. Instead, budesonide induces mitochondrial reactive oxygen species followed by activation of autophagy. Further, the inhibition of autophagy following chloroquine or bafilomycin A1 treatment reduced the anti-viral effect of budesonide against HRV, suggesting that the antiviral activity of budesonide was mediated via autophagy. The results suggest that budesonide represents a promising antiviral and anti-inflammatory drug candidate for the treatment of human rhinovirus infection.

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  • Mon, Jul 06, 2020 - 3:26pm

    jn20

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    Answer to island girl

    First of all the down regulation of MHC-1 by the orf8 protein isn't an all or nothing event. As shown in the article you link to, there some MHC-1 still present on the cells albeit significantly less, likely this makes it harder for the body to initiate an immune response. Prior exposure to a vaccine, will most certainly help as it will prime T-cells to react rapidly upon recognizing MHC-1 loaded with viral derived peptides. The fact that infected cells may have fewer MHC-1 complexes, can of course make it less likely that the MHC-1 complex with viral peptides is recognized. None the less, you should be better of with primed T-cells due to vaccination, as long as you don't stimulate an immune response towards self-peptides (eg an autoimmune response).

    The spike protein is absolutely the best antigen on the virus, especially the highly conserved part responsible for binding to the human ACE2 receptor. If the we can stimulate production of antibodies inhibiting binding of the spike protein to ACE2, we can significantly impair the infectivity of mature viral particles. Additionally, the antibodies may help kill infected cells if they bind to antigens on the cell surface and trigger the complement cascade.

    I would assume that most vaccines use some variant of the spike protein or induce production of some variant of the spike protein. Our antibodies can only recognize surface features of intact viral particles and infected cells, so the antigen need to be extracellular. Likewise, T-cell response due to recoqnition of  MHC-1 with viral derived peptides require an intracellular peptide being loaded into MHC-1. The ideal vaccine against SARS-CoV-2 should initiate both T- and B-cell response for maximal protection.

    Hope it helps,

    Jeppe

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  • Mon, Jul 06, 2020 - 3:42pm

    jn20

    jn20

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    Relax...

    I do not fear most of the chemicals you mention, why? Because dosage, pharmacokinetics and toxicity needs to be tested prior usage on the general population.

    Like any other medicines, vaccines are put through animal studies and clinical trials.

    Phase 1 to investigate safety profile of various dosages based on animal data.

    Phase 2 to investigate efficacy and safety in a small group.

    Phase 3 to investigate and prove efficacy and safety in a large group and investigate risks/benefits of treatment.

    My only major concern is that we rush the deployment of vaccines without a full phase 3 studies. If we do so, we risk that the cure could be worse than the disease.

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  • Mon, Jul 06, 2020 - 4:40pm

    #44

    sand_puppy

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    Ron Paul: Definition of a counted "case" is changed to cause a spike

    Ron Paul, a well know libertarian, is opposed to government edicts and is especially allergic when fudged numbers are used to justify those edicts.  In Texas, the rising numbers of "cases" is being cited to justify governmental restrictions.

    .

    Shifting the definition of a "case"

    Texas State Department of Health Services changing the definition of what constitutes a “Covid case” .... [causing] the mainstream media [to declare] that a “second wave” was on the way ... and that cases were "spiking."

    ...on May 18th, it was revealed that while previously the determination of a Covid “case” was a confirmed test result, the definition was suddenly changed to count “probable” cases as “cases.” At the same time, the threshold for determining “probable” was lowered to a ridiculous level.

    As Judge Hill said at that May 18th meeting, “If you have a subjective fever ["I feel hot"] and you have a headache and you live in Collin County, you now meet the qualifications to be a probable COVID patient.

    And “probable cases” were considered cases.

    Even worse, once a “probable” case was determined based on possibly unrelated subjective criteria, up to 15 people in possible contact with that “probable” case were also listed as “probable cases.” And “probable cases” were considered cases.

    ...Is it any wonder there was a “spike” in “cases”?

    This confirms my impression that it is best to count hospitalizations and deaths as the number-of-cases metric is just too easy to fudge.

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  • Mon, Jul 06, 2020 - 4:57pm

    #45
    JWhite

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    Thymosin Alpha 1 (Tα1) Reduces Mortality of Severe COVID-19 patients; also used as a prophylactic

    A Belgian doctor sent an email advocating the use of Thymosin Alpha 1 in the treatment of SC2, and indicating it ‘decreases mortality by 66% in severely affected COVID patients’.

    Here is a small retrospective study from Wuhan of the use of Thymosin Alpha 1 in Sars-Cov2 treatment:
    Thymosin Alpha 1 (Tα1) Reduces the Mortality of Severe COVID-19 by Restoration of Lymphocytopenia and Reversion of Exhausted T Cells

    https://pubmed.ncbi.nlm.nih.gov/32442287/

    I also came across this short article, which indicates the peptide was also used as a prophylactic with classic SARS in China:

    https://covid19immune.com/articles/peptides/thymosin-alpha-1

    Some highlights:

    Thymosin α 1 (Tα1) is a naturally occurring 28-amino-acid peptide originally isolated from thymus. It acts both as an immune modulator and direct-acting effect.1
    Tα1 has been widely used and tested in a broad range of clinical applications including viral, fungal and bacterial infectious diseases, cancer and as a vaccine enhancer.
    Due to its biological properties and safety profile Tα1 could be used as a protective agent in the elderly subjects with a higher susceptibility to infectious diseases.

    Many people in China used Tα1 as a prophylactic agent against SARS-COV during the 2003 pandemic.2

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  • Mon, Jul 06, 2020 - 4:58pm

    Island girl

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    Thanks for the very clear respone

    Thanks for clarifying. I was able to understand the details of your response, much appreciated. It is encouraging. Have you looked at the German study that speculated prior exposure to other coronaviruses might have  boosted T-cell response to SARS Cov-2? Do you think it means anything for those who get regular flu shots?

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  • Mon, Jul 06, 2020 - 5:15pm

    sofistek

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    Probable cases

    New Zealand report "probable" cases, also. It's definition of a probable case is:

    A probable case is one without a positive laboratory result, but which is treated like a confirmed case based on its exposure history and clinical symptoms.

    This can catch false negatives (which could be 20%-30% of tests, according to our Director General of Health) and cases where a test just can't be done (e.g. with small children or dementia patients).

    We haven't had a probable case for so long that it's stopped being mentioned in updates, though they still appear on our official tally.

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  • Mon, Jul 06, 2020 - 6:35pm

    #48
    Island girl

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    Thanks for the info on inhaled steorids Jim H

    Those are interesting studies!

    The UK found that oral or IV dexamethone helped their NHS patients who were under respiratory distress.

    https://www.recoverytrial.net/files/recovery_dexamethasone_statement_160620_v2final.pdf

    Chris's videos have reviewed the MATH protocol, which also employs a steroid in hospitalized patients.

    The Japanese study referred inhaled ciclesonide in three patients with pneumonia.

    With regard to the Texas doctor using budesonide, wasn't entirely clear to me what the status of his patients were (but I didn't watch the whole video).

    This "rapid review" looked at the data on both ciclesonide and budesonide, but the in vitro data from a single study didn't support an antiviral or anti inflammatory mechanism for budesonide.

    https://www.cebm.net/covid-19/inhaled-corticosteroids-a-rapid-review-of-the-evidence-for-treatment-or-prevention-of-covid-19/

    So  it looks like inhaled steroids might help people in respiratory distress, but we need more data on budesonide, it seems. Maybe the doctor could write up a case series with the pertinent details on his patients. He is obviously excited about what he is seeing.

    Wonder if there is any information on COVID in people with asthma who use inhalers or nebulizers. I would think they are at high risk due to a preexisting condition, but on the other hand, what if COVID symptoms prompt use of their inhalers earluy on -  does that make any difference?

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  • Mon, Jul 06, 2020 - 6:44pm

    #49
    Island girl

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    A review of the series of events in Wuhan

    https://www.bbc.co.uk/news/extra/ewsu2giezk/city-of-silence-china-wuhan

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  • Mon, Jul 06, 2020 - 6:46pm

    #50
    Island girl

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    Correction re post 48

    To clrify: This "rapid review" looked at the data on both ciclesonide and budesonide, but the in vitro data on budesonide didn't support an antiviral or anti inflammatory mechanism

    https://www.cebm.net/covid-19/inhaled-corticosteroids-a-rapid-review-of-the-evidence-for-treatment-or-prevention-of-covid-19/

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  • Mon, Jul 06, 2020 - 6:51pm

    Jim H

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    Island Girl, Rapid review paper

    Thank you for the reference.. but I am confused about your comment relative to it;

    This "rapid review" looked at the data on both ciclesonide and budesonide, but the in vitro data didn't support an antiviral or anti inflammatory mechanism

    But here's what the paper says, and it seems like the opposite of what you are saying above, at the case of the Japan steroid;

    The authors compared the drug effectiveness of ciclesonide, an inhaled corticosteroid medication used to treat asthma and allergic rhinitis, against the drug effectiveness of chloroquine, lopinavir and remdesivir as reference drugs. They found that ciclesonide had an IC50 of 4.33 μM, which was much lower than that of chloroquine (9.12 μM), lopinavir (7.28 μM) and remdesivir (11.41 μM). The authors therefore proposed that ciclesonide exhibits a direct acting anti-viral activity in addition to its intrinsic anti-inflammatory function.

    So ciclesonide sounds like the bomb, no?

    Edit:  I see you corrected yourself... Thank you again for the paper.

     

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  • Tue, Jul 07, 2020 - 7:24am

    davefairtex

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    "probable" cases are cases!

    Where "probable" has a suddenly new and more flexible definition.

    Wow.  That's a scam.  To say the least.

    If we look at this from another viewpoint, however, it is the mark of desperation.  If deaths continue to decline, while cases scream higher, the pandemic will start to seem like a real nothing-burger due to the rapidly declining CFR.

    "Everything that happens in an election year - is about the election."

     

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  • Tue, Jul 07, 2020 - 9:57am

    #53
    Mohammed Mast

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    So Much for Herd Immunity

    It looks like it disappears pretty quickly if you have a mild case. Also it looks like Spain has not come anywhere near 60% exposure.

    https://www.businessinsider.com/coronavirus-antibodies-study-herd-immunity-unachievable-spain-2020-7

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  • Tue, Jul 07, 2020 - 10:57am

    Quercus bicolor

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    So much for herd immunity?

    Yes, but why did the people who tested negative or later tested negative have a mild case?

    1. Was their immune response primarily or entirely not an antibody response (i.e. the T-cell response that has been documented)?  If so, why wouldn't they just respond the same way with a mild response next time?  Why wouldn't it be even milder because of some undetectable or not tested residual immunity?
    2. Was it due to a low innoculum?  In this case, one might expect a more severe case next time.   On the other hand maybe there is some residual immunity that would make this less likely.  Or some hidden damage from round one could make it more likely.
    3. How many people never tested positive, had a mild or very mild case and now have no detectable antibodies?  Why couldn't their next exposure result in exactly the same outcome?

    Of course, there is also the question of a mutation making immunity less relevant in wave 2 or of ADE.

    Sweden will reveal much in coming weeks.  The highest death rate for any country is still under 1 out of a thousand people and all but Belgium are near or below one out of 2000.  How many of these are elderly people who would have died from another cause within a few weeks to a year or so?  How many people might be hurt or killed by another lockdown?  Would mask wearing, reasonable efforts at distancing and, of course, HCQ given early (including to those elderly people who survived wave 1) be the best response?  How could the story in the BI article serve those with a vaccine agenda?  Lots of unanswered questions.

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  • Tue, Jul 07, 2020 - 11:25am

    #55
    JWhite

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    Why It Matters if SC2 Came From a Lab

    In thinking about the question of why the origin of the SC2 virus matters, I would add that it matters because > 500,000 people have died (so far), > 11 million have been infected by the virus (so far), and countless others have had their livelihoods impacted.  Someone, or some individuals need to be held accountable.  If the pandemic was naturally occurring, then we could accept it, but if it was man-made, then it is not acceptable.  Blame must be laid!

    Australia has pushed for an independent investigation into the origin of the virus, and the handling of the pandemic.  This is very important and hopefully it goes forward.

    https://www.sbs.com.au/news/coalition-of-116-countries-back-australia-s-push-for-independent-coronavirus-inquiry

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  • Tue, Jul 07, 2020 - 5:09pm

    #56
    nordicjack

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    No herd immunity on this one

    Even if you got to 50% , you would quickly start loosing immunity as well.   Until everyone gets this 2 times per year , which is what I think the vaccine will require about 3-4 years of 2x /yr    before this is really put away.     That is a lot of taxing the immune system.  I do not believe in vaxxing.  But for older people , and sick people , there may be no choice , even young people , there may be no choice.    problem is older people do not build antobodies and react as strongly to vaccines ( flu ) as younger healthy people.. So will it even work with them? or can be more like the flu, it will not work as well in the people who need it.   But this may be the best argument to vax younger people.. as to protect the older people.. who are technically minimally vaxable.

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  • Tue, Jul 07, 2020 - 7:53pm

    Island girl

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    Why It Matters if SC2 Came From a Lab

    To add to the point made by JWhite on how this has affected all of us.

    First, we pay for this research. For example, the research published in 2015 paper on chimeric Frankenviruses was funded by NIH (specifically NIAID, headed by Dr. Anthony Fauci), National Natural Science Foundation of China, and the NGO, EcoHealth Alliance, which gets funding from USAID and NIH. We, the public, funded this, they are accountable to us.

    Second, as this community knows, this GOF research is very dangerous because of the pandemic risks that accidental release would pose. Because of objections raised within the scientific community, the research was "paused" in 2014 and "resumed" in 2017. Here's what the article cited above states:

    Experiments with the full-length and chimeric SHC014 recombinant viruses were initiated and performed before the GOF research funding pause and have since been reviewed and approved for continued study by the NIH.

    So whoever decided this was a good idea despite the risk should be held accountable .

    Third, because people affiliated with this research (such as Dr. Peter Daszak, President of Ecohealth Alliance) have been saying to the media that there is no way this could have come form a lab, even though they have been finding this very research into genetically engineered viruses that posed a risk of escape. This characterization is misleading, to say the least. Those decisionmakers who are directly involved but silent, those who conducted the research but are silent, and those surrogates who are involved but saying "nothing here to see",  should be called out.

    This CNN headline from 2017 is pretty direct:

    https://www.cnn.com/2017/12/19/health/nih-deadly-viruses-bn/index.html

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  • Tue, Jul 07, 2020 - 9:25pm

    #58
    Island girl

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    Recombinant SARS Cov viruses with certain features of SARS Cov-2 have been engineered in a lab

    So here's a timeline:

    In this paper from 2013, Dr. Peter Daszak, Dr. Shi and colleagues isolate and characterize a SARS-like coronavirus from Chinese horseshoe bats from a cave in Yunnan province (some distance from Wuhan). They discover that, like the epidemic strain SARS-Cov-1 (but unlike other SARS-like coronaviruses), the spike protein of this isolate binds human ACE-2. They name this bat SL-CoV-WIV1 (initials seem obvious).

    https://www.nature.com/articles/nature12711

    we report the first recorded isolation of a live SL-CoV (bat SL-CoV-WIV1) from bat faecal samples ...which has typical coronavirus morphology ... and uses ACE2 from humans, civets and Chinese horseshoe bats for cell entry...Our results provide the strongest evidence to date that Chinese horseshoe bats are natural reservoirs of SARS-CoV, and that intermediate hosts may not be necessary for direct human infection by some bat SL-CoVs.

    I would note that bats were not sold in the Wuhan market and that the above bat SARS-like virus (WIV1) uses human ACE-2 receptor and needs no intermediate host.

    Next is the 2015 paper cited in previous posts, in which Dr. Shi and colleagues create a chimeric SARS Cov virus with a distinct S protein and a SARS Cov genetic backbone, and show that it infects and replicates in human lung cells, causes pathology, and is recalcitrant to neutralization by antibodies because of its novel spike protein.

    https://www.nature.com/articles/nm.3985

    In 2017, after 5 years of surveillance studies in bat caves, they identify 11 more SARS-like strains from bats in Yunnan province, which differ significantly in the S gene and the ORF8 reading frame, among other sequences.

    https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1006698

    (I mention these in particular because in SARS Cov-2, the S protein is the key that unlocks the ACE-2 receptor and the ORF8 down regulates MHC expression on human T cells, which would reduce the degree to which these immune cells recognize the virus as foreign).

    Much of the paper is devoted to genetic characterization, but one section is noteworthy from our standpoint:

    Using the reverse genetics technique we previously developed for WIV1 [presumably the 2013 isolate], we constructed a group of infectious bacterial artificial chromosome (BAC) clones with the backbone of WIV1 and variants of S genes from 8 different bat SARSr-CoVs  

    So they constructed artificial chromosomes containing the genetic backbone of the bat SARS-Cov WIV1 (that they believe was the progenitor to SARS-Cov-1) but with various different spike protein genes spliced in. So 8 chimeras. (It has been asserted in the press that this technique does not leave a signature of artificial manipulation).

    Two of the eight chimeras were cytotoxic to monkey cells, so evidently they obtained replicable virus via the technique of infecting with artificially reconstructed bacterial chromosomes containing the requisite viral genes.

    When Vero E6 [monkey] cells were respectively infected with the two successfully rescued chimeric SARSr-CoVs, WIV1-Rs4231S and WIV1-Rs7327S, and the newly isolated Rs4874, efficient virus replication was detected in all infections.

    The two engineered viruses, and an additional wild-type virus, were able to use ACE-2 receptor to infect human cells.

    To assess whether the three novel SARSr-CoVs can use human ACE2 as a cellular entry receptor, we conducted virus infectivity studies using HeLa cells with or without the expression of human ACE2. All viruses replicated efficiently in the human ACE2-expressing cells.

    Conclusion: I think we can conclude that many SARS-Cov viruses have been engineered in a lab, and some of the details have been published.

    This group first discovered a SARS-Cov virus from bats that infects human cells directly via ACE-2, then artificially engineered this SARS Cov-1 type virus by manipulating the spike protein in multiple ways over time. Various artificial chimeras were produced that infect human cells via ACE-2, replicate efficiently in human cells, cause pathology, and in some cases resist neutralization by antibodies.

    We know that in SARS Cov-2  has a SARS Cov backbone and a spike protein distinct from the SARS Cov-1; and that the S gene includes a 12-base-pair insertion for a cleavage site that makes the spike protein  effective at using ACE-2 for cell entry.  SARS Cov -2 also has differences in other sequences, such as ORF8, which these researchers found to be diverse in different bat corona viruses. Could SARS Cov-2 have come from a lab? Of course the possibility exists. Engineered SARS-Cov viruses made in Wuhan are a reality, not a hypothetical.

    Just as an aside, interesting to see how far Yunnan province, site of the bat caves, is from Hubei Province where Wuhan is situated.

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  • Tue, Jul 07, 2020 - 11:00pm

    Dr. Jurgen Mayer

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    Dr. Jurgen Mayer said:

    pCoV-MP789 from Malaysian Pangolins found close to the Yunnan border + RaTG13/4991 from Rhinolophus Affinis bats found in Yunnan province + cleavage site insertion and we are done.

     

    Accessions pCoV (MT121216), RaTG13 (MN996532) and it's original RdRP of 4991 (KP876546)

     

    No need for a SARS-CoV backbone or anything else. These three items match nCoV-2019 by 99.6%. Even SL-CoV ZC45 (MG772933) has a better binding affinity than SARS-CoV, so there is absolutely no need to use the SARS-CoV backbone when much better candidates exist.

     

    While I can prove this was made in a lab, I cannot prove which lab or country this came from.

     

    Also and for clarity, RaTG13 came from 870 miles west of Wuhan. WIV01 (KC881007) was not the basis for SHC014 (KC881005) nor was it the basis for hACE binding. That was SL-CoV-Rs3367 (KC881006) as referenced in the original 2013 publication.

     

    Rs3367 (Rs being Rhinopolus sinicus, commonly found in Yunnan) was sampled on 19, March, 2012 whereas WIV01 was sampled 18, September, 2012. They were both used in the publication but 3367 was the basis of their research in 2012. After their findings, they pushed SHC014 for chimeric adaptation. Nonetheless, all 3 viruses come from the Chinese Rufous Horseshoe Bat (Rs).

     

    The bigger story is that RaTG13 was discovered as SL-CoV-Ra4991 3 months before the 2013 publication was submitted. No chimera required there!!

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  • Wed, Jul 08, 2020 - 3:02am

    #60

    sofistek

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    More bad news on the effects of Covid-19

    Warning of serious brain disorders in people with mild coronavirus symptoms.

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  • Wed, Jul 08, 2020 - 5:26am

    VeganDB12

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    effects of Covid in "mild" illness

    Sofistek that is a scary notion, brain disease from mild disease. And I don't question the findings as such.  It may not be obvious to some (maybe to people here) but it is incredibly difficult to address issues in milder illness because these patients are sent home to recover once they test positive. We know a lot about ICU patients but our knowledge of ambulatory patients will take a long time to acquire.  I believe the reason is the mandated isolated of patients, which is necessary, and shutdown of the outpatient centers where these workups are done. Mainly because of isolation requirements.  This seems obvious but is having a big impact on what we know about mild disease. It could take years to get this data. Thank you for the article I know if I can find this information anywhere it will be here.

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  • Wed, Jul 08, 2020 - 11:28am

    #62
    tbp

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    Serious brain disorders in people with mild coronavirus symptoms?

    @nordicjack
    I do not believe in vaxxing. But for older people , and sick people , there may be no choice , even young people , there may be no choice. problem is older people do not build antobodies and react as strongly to vaccines ( flu ) as younger healthy people..

    There is always a choice on whether you're willing to inject aluminum into your own body. (Almost every single vaccine contains it, the manufacturers admit it, but criminally-negligent doctors don't tell you.) It's about the worst thing you could ingest. It's healthier to consume a SAD diet for a year, maybe 10 years, than to take a flu shot or other trojan-horsed adjuvanted vaccine.

    @sofistek
    Warning of serious brain disorders in people with mild coronavirus symptoms.

    Where these people vaccinated (and thus their terrain/immunocompetence destroyed)? What's their vitamin D status? (Maybe even 'How long were they socially isolated?' because loneliness / psychological distress translates to chronically elevated baseline cortisol levels which translates to immune system shutting down.) Without those questions, never asked in clownworld, it's difficult to attribute causality to the virus itself.

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  • Wed, Jul 08, 2020 - 12:05pm

    Island girl

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    Thanks for the expert perspective WODZ

    It appears you conclude that SARS Cov-2 was engineered but not in manner described int the published studies that I cited.

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  • Wed, Jul 08, 2020 - 1:05pm

    stevedaly

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    Reply to WODz #59

    Why do arguments against the theory of COVID-19 development in a laboratory never consider the pangolin virus GD Pangolin CoV?

    In Dr. Martenson’s discussion of the origin of the COVID-19 virus he compared the GD Pangolin CoV virus to COVID-19 (SARS-CoV-2)

    “When we do, we discover that - hands down! - the all-important receptor binding domain (RBD) came from a pangolin, not a bat.

     

    “It's not even a contest.  The pangolin/1 has 5 out of 5 all-important RBD contact amino acids (AAs - red boxes) in common with the pangolin, and 8 out of 9 adjacent AAs (yellow boxes).   It's closest 'bat relative' - RaTG13 only scores 1/5 for RBD contact, and 4/9 adjacent AAs.   The other bat  coronaviruses and SARS-classic are far worse.”

    So why didn’t Daszak or Anderson et al. in their NatureMedicine article claim that COVID-19 developed naturally from the pangolin virus?  They are silent on this possibility.  Is it because pangolins don’t have communities like bats that permit passing viruses back and forth to develop mutations?  According to Wikipedia, “Pangolins are solitary and meet only to mate.”

    And they are endangered.

    https://en.wikipedia.org/wiki/Pangolin

     

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  • Wed, Jul 08, 2020 - 5:20pm

    jn20

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    jn20 said:

    It is at a minimum equally likely to the "bat/pangolin" crossover hypothesis that the mutations from the pangolin virus was introduced into RATG13 by site directed mutagenesis on a plasmid encoding the entire viral genome. This a technique commonly used in molecular biology laboratories and is at a minimum equally likely. Also, consider how long both the pangolin virus and RATG13 was known by the chinese prior to SARS-COV-2...

    Another way for RATG13 to accumulate the same mutations, would be by directed evolution. Here, the virus is cultured together with cells expressing human ACE2, only viruses with strong binding to human ACE2 will proliferate and rapidly mutations increasing binding to human ACE2 will accumulate.

    I  have been suspicious for a long while now and I support Chris on the lab origin. While it is rapidly dismissed by ordinary people as another conspiracy theory, I as a Molecular Biologist have had my suspicion for months... In my opinion we are looking at an accidental release, likely due to a lab technician or a scientist accidentally getting infected. They likely wrote it off as a common cold/flu and decided not to reveal their mistake... It is China after all and who knows what would happen to you if you make a stupid mistake. It wouldn't be the first time a mistake happens in a lab and neither will it be the last...

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  • Wed, Jul 08, 2020 - 5:52pm

    #66
    Island girl

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    Thank you for your posts WODZ, Steve Daly, and Jn20

    Perhaps one of you could explain in terms that a non-molecular biologist can follow, I get the gist of what you are saying but I - and perhaps others in the community - would be interested in the family tree of SARS-COV2 and the derivation of its critical features.

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  • Thu, Jul 09, 2020 - 6:46pm

    Dr. Jurgen Mayer

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    to stevedaly

    Q: Why do arguments against the theory of COVID-19 development in a laboratory never consider the pangolin virus GD Pangolin CoV?

    A: For clarification purposes, there is no such thing as the GD Pangolin CoV. GD is specifying Guangdong province of China. Malaysian Pangolins are typically smuggled into Guangdong, Guizhou, Guangxi, or Yunnan provinces but predominately into Guangdong to Shenzhen or Guangzhou cities. The relevant pCoV viruses that I believe you are referring to are actually from the Guangxi autonomous region. Those viruses are designated as GX. The GenBank accessions are PCoV_GX-P4L (MT040333), PCoV_GX-P1E (MT040334), PCoV_GX-P5L (MT040335), PCoV_GX-P5E (MT040336), PCoV_GX-P2V (MT072864). The Spike protein of RaTG13 has a higher match and furin score compared to any Pangolin virus on record, so we would deduce that the initial proximal zoonotic origin would be that of a bat and not a pangolin.

     

    Q: In Dr. Martenson’s discussion of the origin of the COVID-19 virus he compared the GD Pangolin CoV virus to COVID-19 (SARS-CoV-2): “When we do, we discover that - hands down! - the all-important receptor binding domain (RBD) came from a pangolin, not a bat. It's not even a contest.  The pangolin/1 has 5 out of 5 all-important RBD contact amino acids (AAs - red boxes) in common with the pangolin, and 8 out of 9 adjacent AAs (yellow boxes). It's closest 'bat relative' - RaTG13 only scores 1/5 for RBD contact, and 4/9 adjacent AAs. The other bat coronaviruses and SARS-classic are far worse.”

    A: This information is correct. The amino acid residues in question are L455, F486, Q493, S494,N501, and Y505. These six key positions within the Receptor Binding Domain portion of the Spike protein have been suggested to increase virulence as well as promote a firmer reception. The Malaysian Pangolin virus in question is actually pCoV-MP789 (MT121216) which was sampled from a wild Pangolin in southern Yunnan province, quite close to the Malaysian border. Although these key amino acid residues play a role with virulency, there are only part of a much larger puzzle. The abscense of these 6 residues would simply weaken the virulency of nCoV-2019. Think of these as a specialized icing on the cake. The S1/S2 section is the true gem of this virus. When scoring the RBD region we actually find that RaTG13 is 86.19% similar to nCoV-2019 whereas pCoV-MP789 is 86.64%. Breaking down the specific differences within the RBD of each virus plays out the entire picture. More importantly, the Spike protein of RaTG13 scores 93.15% similarity to nCoV-2019 compared to only 84.52% from pCoV-MP789. The latter being the second higher scoring Spike comparison to this novel virus. We should consider the potency of the the RaTG13 spike protein as more significant than pCoV-MP789 while simultaneously accepting the 6 amino acid residues within the RBD of pCoV-MP789 provide higher virulency. Does this make sense? Both have their merits and nCoV-2019 appears to be a blend of the two.

     

    Q: So why didn’t Daszak or Anderson et al. in their NatureMedicine article claim that COVID-19 developed naturally from the pangolin virus?  They are silent on this possibility.

    A: RaTG13 is by far the closest match, across the board. You need to take all proteins into consideration here. We cannot cheery pick. The RBD section of pCoV-MP789 is the only nod we can provide and even that is only a 0.45% differential. Both the Spike protein (93.15/84.52) and the ORF1ab (96.52/90.36) are clear indicators that a Rhinopholus Affinis bat is the probable zoonotic origin of nCoV-2019. In zoonotic viral recombinant process, we would expect the overwhelming majority of source RNA to be from the origin and only a fractional minority to be from the secondary source (Pangolin). A(primary)+B(secondary)=C. Does this make sense? Given the existence of RaTG13, it would not even make sense to suggest a Malaysian Pangolin as the single source of this virus.

     

    Hope this was helpful information 🙂

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  • Thu, Jul 09, 2020 - 7:31pm

    #68

    sand_puppy

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    Jurgen Mayer, where did the virus come from? Best guess.

    I appreciate you ideas and thoughts.  Sounds like you have lots of experience in this field.

    Can you give us your best guess on where the virus came from.

    Then, in a separate section, discuss the reasons for your conclusions.  (This might help to separate out the technical details that most of us cannot understand or follow easily.)

     

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  • Thu, Jul 09, 2020 - 7:50pm

    Dr. Jurgen Mayer

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    island girl - photogenic tree

    Perhaps one of you could explain in terms that a non-molecular biologist can follow, I get the gist of what you are saying but I - and perhaps others in the community - would be interested in the family tree of SARS-COV2 and the derivation of its critical features.

    In terms of the family tree, we would need to really dig down. We are way way down in sarbecovirus, which is a lineage of betacoronaviruses, which is a genus of coronaviruses.

    Let's say there are 4 different root families for coronaviruses; Alpha, Beta, Gamma, Delta. Let's then say that the overwhelming majority of live coronaviruses in the world stem from Beta. Once we dig into Beta we have 4 lineages; let's call these A, B, C, D. Two of the common colds, hCoV-OC43 and hCoV0HKU1 come from A. SARS comes from B. MERS comes from C. D is boring. Here is a tree outlining what I just described.

    Virtually all bCoVs come from bats as they are natural reservoirs for viruses. Various viruses can live in bats for their entire lives with little to no impact to the host. This is also why Bats and not Pangolins would be the likely "source" as the viruses tend to have physical impacts on Pangolins and shorter their life span.

    In this photo, you can see a partial phylogenic tree on the right side sorting various viruses based on complete genomes (nucleic acids). We use databases and software tools to compare genomes and these trees are comparative groupings. You can see BetaCoVs and Alphas listed there. The purpose of this specific chart was to underscore the similarity of nCoV-2019 to RaTG13, ZXC21, and ZC45. All of three of those listed viruses have controversial histories and genomes. You can spot SARS-CoV on the top.

    When it lists SARSr, that means SARS related virus. Capitalized letters after the initial description denote a city name. Capitalized first letter and lower case second letter indicate the name of the specie they retrieved samples from

    Bat-SARSr-Rs672: SARSr (SARS related, but was previously classified as SL or SARS-like). CoV (coronavirus). Rs (Rhinopolus sinicus, also known as the Chinese rufous horseshoe bat which is found in the Yunnan province of China, India, Vietnam, and Nepal). 672 is the sample number.

    Another example: Bat-SARSr-CoV-ZXC21 and ZC45. I will do an entire post on these crazy viruses but the breakdown here is that ZC stands for Zhoushan City in Zhejiang, China. Whereas ZXC21 was discovered at a nearby mountain, so to avoid confusion they designated that site as ZXC as opposed to ZC.

    Here is a Beta tree that includes the MP789 pCoV (listed as Pangolin-CoV 2020, even though it is from 2019). This tree scoring is the same as the previous, comparing NA of entire genomes. The "groupings" should be obvious to spot.

     

    In terms of the key features of nCoV-2019 compared to SARSr CoVs that would require a much longer response. The KEY takeaway is that nCoV-2019 has a unique RNA insertion at a VERY crucial position that plays a vital role. That "type" of mutation is absent in ALL other betacovs (except one but lets ignore that lol).

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  • Thu, Jul 09, 2020 - 8:00pm

    stevedaly

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    Dr. Mayer

    Thank you Dr. Mayer.  You have my deepest appreciation for what you are sharing with us.

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  • Thu, Jul 09, 2020 - 8:08pm

    Dr. Jurgen Mayer

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    sand_puppy - origins

    Q: Can you give us your best guess on where the virus came from.

    A: The most probable origin is a chimeric virus created in a laboratory. Which lab or country would be complete speculation.

     

    I focus on the science and not the news. The science is telling me that this virus was put together. The basis of the virus "appears" to be the RaTG13 virus. Why? Because that is the closest relative to nCoV-2019. This virus comes from a specific bat species in southern China and is not sold or found in wet markets. The second closest relative is a Malaysian Pangolin. Although this animal is sold/consumed in wet markets, last year scientists discovered a new betacoronavirus found in a specific Malaysian Pangolin. Neither of these two viruses could form nCoV-2019 but if we were to merge these two viruses then we would be around 98.9% identical. Does that make sense? The Bat virus has key features that the Pangolin virus does not have, while it is also true that the Pangolin virus has features that the Bat virus does not have. nCoV-2019 possesses all of these "features" since the original genome sequence. Aside from all of that, nCoV-2019 has this 1 specific SUPERMAN feature that no other betacoronavirus possesses; including the aforementioned Bat and Pangolin viruses.

     

    How about this; I write an essay and then hand it to you for annotations and edits. I am the primary source (Bat) and you are the secondary source (Pangolin). In Microsoft Word we can track changes and can determine who wrote what and where the overlaps are. There is also some gibberish inserted into the document because you and I are sort of bumping heads as our papers are being mushed together. That gibberish is useless. But while reviewing the paper, we discover an entire paragraph written in Japanese. You did not write that. I did not write that. The gibberish mush could not have created it. Where did that paragraph come from? Hopefully that makes sense. This key SUPERMAN feature in nCoV-2019 no origin. It is absent in all Bat viruses and all Pangolin viruses. It is impossible to overstatement the significance of this feature. So the "location" of this feature cannot have been accidental. There are only two conclusions; either someone in a lab put it there or GOD himself stepped in to destroy evolution and genetics. To find this feature in this virus right from the start and not be able to determine the original host animals... you have a better chance of winning the lottery 50 times. Nature does not work like this. For clarification, this superman feature is missing in both SARS and MERS.

    This feature superpowers the virus in terms of how it can spread in cells. The Flu, Common cold, Ebola, Zika, and Yellow Fever all have this. We both know how contagious and rampant the flu and common cold are. The existence of this within nCoV-2019 means this is a super virus.

     

    Hopefully this has been helpful, I tried to keep it non-technical. 🙂

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  • Thu, Jul 09, 2020 - 10:12pm

    TurquoiseRose

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    Have you reviewed Luc Montagnier and Perez's information?

    COVID-19, SARS and Bats  Coronaviruses Genomes
    Unexpected Exogeneous RNA Sequences

    By Luc Montagnier, 2008 Nobel Prize in Physiology or Medicine for his discovery of the human immunodeficiency virus.
    Jean-Claude Perez, PhD Maths § Computer Science Bordeaux University, RETIRED interdisciplinary researcher (IBM Emeritus, IBM European Research Center on Artificial Intelligence Montpellier), Bordeaux metropole, France

    https://osf.io/d9e5g/

    "We cannot apply the current and proven tools and methods of fighting against viruses, hitherto NATURAL, because we do not know today how a new virus whose part of the genome is SYNTHETIC in nature will evolve.

    • This was already true for SARS, and even more so for COVID-19."     
    • This preprint was last updated 4.25.20. I would love your comments. TR

     

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  • Thu, Jul 09, 2020 - 10:53pm

    Dr. Jurgen Mayer

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    Montagnier

    There are indeed a number of residues in this virus that present HIV homology. This is how I like to describe this virus in non-technical terms.

     

    For our example, we will call the virus a car. By virus though I am very specifically talking about aspects of the Spike protein. Each car in this example represents a different protein in the human body that naturally serves different purposes. Through extended evolution (years or decades) a virus can gain new abilities and learn to deal with new cars.

    SARS-CoV was like a thief. It could only target Honda cars. It then had to break the car window and manually attempt to hotwire the car. Not very efficient and this was only working some of the time.

    MERS-CoV had the same problem with Hona cars but had the keys to Toyota cars. With Toyota cars, it could unlock the car, turn on the ignition, and drive away.

    hCoV-2019 came with keys to 6+ car brands. This is beyond suspicious. This virus does not need to hotwire these cars. Sometimes the key does not work properly but let's say it has many sets of Honda keys, so it can use many attempts to hijack that car. This is a super virus. One of the cars is called CD4. Without going into detail, let's call this one of the primary T-cells for the immune system. HIV uses its GP160 protein receptor as a car key to enter CD4 and infect the host with HIV. While hCoV-2019 cannot give a host HIV nor does the virus contain traces of the HIV (virus), it has the "same" car key to access CD4. This is what Dr. Montagnier and his team were examining in their research. We believe a CD4 receptor hijack would weaken the immune system of the host and the host would potentially both test false-positive for HIV and present with "HIV-like symptoms" in the sense of immune deficiency.

     

    This is very important research and only a few around the world are taking this seriously. Why? Because no scientist wants to admit the reality that this virus came with 6 car keys.

     

    Everyone needs to avoid this virus as best they can. This is not a respiratory virus like SARS but a honey badger virus that can and will try to attack every organ in your body until you submit.

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  • Fri, Jul 10, 2020 - 4:59am

    #74

    sand_puppy

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    Appreciate the car keys analogy

    For a non-technical person, that analogy gives me a starting point to understand what you are talking about.  Thank you.

    My understanding of what you just said:

    The "keys" in this analogy are receptor docking and access capabilities.

    The "cars" are different cell types.

    And this nCoV-19 is able to enter many different cell types.

    nCov-19 is like a highly trained thief who was taught this trade by a team of master thieves called in to train him how to break into each different cell type.

    This concentration of expert thievery skills (into so many different cars) does not occur naturally.

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  • Fri, Jul 10, 2020 - 5:07am

    #75
    KnitKnotKnow

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    Malaysia do not border Yunnan

    Re: Post #67

    ”....The Malaysian Pangolin virus in question is actually pCoV-MP789 (MT121216) which was sampled from a wild Pangolin in southern Yunnan province, quite close to the Malaysian border.  ...”

    Just want to clarify something. Minor but important to me at least. Not downplaying Dr Mayer’s post at all.   The Malayan pangolins are also found in Myanmar which borders Yunnan. Malaysia is way way further down from Yunnan. There’s Thailand that borders Malaysia.

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  • Fri, Jul 10, 2020 - 5:58am

    JWhite

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    Replying to Dr. Mayer

    Dr. Mayer - thank you for introducing yourself in the forum, and for contributing your analysis to this conversation.

    I'm not sure if this is outside the scope of your work, but given the research of this virus by you and your colleagues, do you have any comments on the subject of immunity to the virus, and also the expectation of potential mutations (including the question of immunity to new mutations, for those who were exposed to an earlier strain) ?

     

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  • Fri, Jul 10, 2020 - 11:58am

    Dr. Jurgen Mayer

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    KnitKnotKnow - Pangolins

    Thanks for the correction! That jogged my memory. I had previously stated that the Pangolins were found in Yunnan, next to Malaysia. Incorrect and I was thinking of a different case. For the Pangolin(s) in question, they were being smuggled into China and were seized as Guangdong customs. Sequencing analysis was completed in March and July of 2019 . All three smuggled Pangolins died from severe respiratory diseases.

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  • Fri, Jul 10, 2020 - 12:40pm

    Dr. Jurgen Mayer

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    JWhite reply

     

    Not to scare everyone but a vaccine for this virus is highly improbable. We could not develop a vaccine for SARS, even after 10 years of research. This virus is at least 10x worse. Not the information that people want to hear but our best chance from a scientific angle is to find ways to slow the virus down to reduce symptoms. Everyone wearing masks for an extended period would slowly starve the virus out.

    RNA viruses tend to have many mutations and we have been tracking these in great detail. The problem has been with the lack of sequencing. PCR testing or RdRp sampling cannot determine if a patient has a key mutated version of the virus. Globally, we have genome data on roughly 0.6% of confirmed cases. There are 7 key "groups" of this virus and more will appear over time. I am not referring to mutations but something called clades. Virus-clades-mutations, that gets branched out

    L, S, V, O are clades that have their mutations in the ORF1ab protein of the virus and these various changes can cause patients to present with different symptoms. Korea, Italy and UK, for example, were hit by the V clade. France initially had O and then L. In February we then saw a key mutation in the Spike protein which caused the virus to become more deadly. This is the G clade. GR and GH are essentially G+R or G+H. Aside from having the key (G) Spike mutation these genomes also have (different) mutations in the N protein. Of the genomes that we have on file:

    GR: 16,451

    G: 13,099

    GH: 12,343

    S: 4,017

    V: 3,727

    L: 3,445

    (Other: 2,753)

    *Keep in mind that many countries around the world are not reporting their cases and therefore we are not receiving any genome information. So the global cases and deaths are exceptionally skewed and incomplete.

    G+ is currently responsible for 70% of sequenced genomes. Please keep in mind that these numbers only represent 0.6% of cases.

    As with influenza if a host was infected with strain A, develops anti-bodies then the host would be less susceptible to strain A within X time period. The host would still be susceptible to strain B. This is because each strain has its own unique RNA signature and your immune system has a memory for each signature. A better example is that Border patrol would look at two brothers entering customs. They know to exclude brother 1 (antibodies) but they allow brother 2 to enter because his social security number is different. In reality, these two are not brothers but the same virus, posing as two different "people". Hopefully that makes sense. We are finding that hosts are not currently developing long-lasting immune responses to this virus. This means there is even less likelihood to develop antibodies for A and be protected from B. The good news is that since G+ is the current dominant clade, developing any antibodies against these strains is much better compared to L, V, S, O.

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  • Fri, Jul 10, 2020 - 1:03pm

    Dr. Jurgen Mayer

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    sand_puppy

    You are getting the basis of this, but one important point of clarification

    "nCov-19 is like a highly trained thief who was taught this trade by a team of master thieves called in to train him how to break into each different cell type."

     

    This situation is far worse as the virus came packaged having already mastered all of these aspects. To say this is highly unusual for a virus is a massive understatement. As you suggested, the virus needs to learn a skill and it becomes better over time. How then could this virus be a master from the start? This is one of the reasons why saying this virus naturally "evolved" does not work very well since it appears to have skipped many generations of evolution.

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  • Fri, Jul 10, 2020 - 2:37pm

    robie robinson

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    Dr. Meyer

    Wouldn’t mutations, over time and likely quite long, devolve back to an original “type” without the gain of function developed thru gene editing?

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  • Fri, Jul 10, 2020 - 3:52pm

    Mpup

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    OSF preprint

    Why when I try to decipher the OSF preprint I keep thinking we have a puzzle with more than 10,000 pieces, all which are constantly moving. I suspect the odds of putting in the last piece (vaccine) at just the right moment are infinitesimal.  In the words of Island Girl "chimeric Frankenvirus"   In search of an HIV vaccine, a monster more efficient in spread and killing has been created.  Welcome to the brave new world.  "In thinking themselves wise, they've shown their foolishness"

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  • Fri, Jul 10, 2020 - 4:39pm

    JWhite

    JWhite

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    Replying to Dr. Mayer - Immunity & mutations

    Danke sehr - good information.  So it seems best if we do not count on an effective vaccine, or on lasting immunity.  Dr. Chris's latest video also discusses the observation that immunity seems to be short-lived, if the patient develops it at all.  If we don't expect lasting immunity, and/or the immunity does not extend to new/variable clades, then it seems that 'herd immunity' is also not to be expected in any given society.

    I like the idea of 'starving out' the virus by everyone wearing masks when they are in populated areas.  This may be the best solution, together with hygiene measures....

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  • Fri, Jul 10, 2020 - 4:50pm

    #83

    Oliveoilguy

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    Chinese Covid Whistleblower

     

    She says Herd Immunity is not possible....but does not give much info in this interview.

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  • Fri, Jul 10, 2020 - 7:46pm

    Island girl

    Island girl

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    What makes SARS_Cov 2 so different - am I on the right track?

    Dr. Mayer, thanks for giving us several helpful analogies to try to follow what you are proposing.

    I am intrigued by this and trying hard to follow. Please bear with me, I will share what I think you are saying, then you and others can correct me to clarify for the community. I am not a molecular biologist.

    1. Bat corona viruses and Pangolin coronavirus are from the Beta family of coronaviruses and both are in the lineage B of that family. So in some sense they share commonalities, perhaps different species within a genus, adapted to different hosts.

    2. SARS Cov-2 is most closely related to a specific Bat corona virus, nomenclature Bat Cov RaTG13 (originally called SL-CoV-Ra4991 and discovered circa 2013?). As you say "discovered", did RaTG13 come from the wild? Who discovered it?

    3. Bat corona virus RaTG13  (blue line in chart below) is quite distinct from certain other Bat coronaviruses, the latter of which are in some way pertinent to SARS (green and brown lines). (Pink line is somewhat related to green and brown SARS Cov viruses in regions and somewhat related to RaTG13 in others). Apparently this uniqueness of RaTG13 is very significant. Is that in terms of discerning a direct evolutionary precursor or for some other reason? (I'm guessing here)

    What I state above, I gather from the chart of "nucleotide identity at the same position" pasted below - a chart shared by Dr. Mayer in a link.

    It also looks like there are two places in the nucleotide sequence where RaGT13 (blue line) is very different from all the other coronaviruses in this chart. One is somewhere between 20,0000 -25 ,0000 nucleotides and the other between 25,000 and 30,000 nucleotides. Is there some functional significance to the gene product or gene regulation in these ?

    (You also say, tangentially, that the viruses represented by the colored lines are somehow controversial in the scientific community.)

    4. RaTG13  is related somehow to other SARS WIV viruses named by researchers in the Wuhan lab, but is also distinct in some significant way, because it is on its own "branch"?

    That whole cluster, if you will, is related to "controversial" SARS Cov ZC45 as well as SARS Cov ZXC21. The previous chart shows the areas of similarity between RATG13 (blue line) and ZC45 (pink line).

    5. The next closest genetic relative to SARS Cov-2 is a corona virus derived from Pangolins. Generally speaking, Chinese bats bats from Yunnan caves do not live with Pangolins from Myanmmar. But Pangolins have been smuggled into China. You mention that three smuggled pangolins died of respiratory disease, from which I infer that pangolin coronavirus can be quite pathogenic to its natural host.

    6. There is a Pangolin Cov 2020 virus that is also somehow related to Bat Cov ZC45 and Bat Cov ZXC21.  I gather this from a section of a chart you linked to below. However, the pangolin Cov 2020 resides on its own "branch".

    Looking at the chart further, Bat Cov RAGT13  is somehow related to SARS Cov-2, and Pangolin Cov 2020 connects somehow to both of them.

    I gather all this from the chart below that you linked to. I do not fully understand the relationship indicated by separate and connected branches on the tree.

    Elsewhere in your post, it seems that this pangolin Cov is also called pCoV-MP789?.

    7. If you take some of the features (I assume you mean nucleotide sequence?) of Bat Cov RATG13 and "cut and paste" some of the sequences of Pangolin Cov 2020, you get almost identical genetic sequence to SARS Cov2 that causes COVID-19 (99.6%).

    (I assume cut and paste to preserve viral viability, but perhaps the pangolin features are so circumscribed that they could occur by mutation?)

    Conclusion: In SARS Cov-2, the majority source RNA is Bat and the secondary source is pangolin.

    8. Once you combine Bat SARS Cov RaGT13 and Pangolin Cov 2020 then add a cleavage site (the last 0.4% that is dissimilar perhaps?) you end up with SARS Cov-2.

    Is this correct?

    I have assumed that all along when you talk about similarities you are speaking of nucleotide sequences. The pertinent sequences I assume are either regulatory in nature or produce altered gene products that give us the functionality of SARS Cov -2.

    Please correct any misunderstandings above, I would love to be able to follow what you are proposing.

    Now in terms of functionality of SARS Cov-2:

    You give us an analogy to cars and car keys  and the virus is a carjacker. (By different types of cars, do you mean different types of human cells, or do you mean cells of different species of animal?). SARS Cov-2 can unlock the door and carjack many types of cars.

    Now I have a new question:

    9. Can you explain what functionality the (1) bat aspects, (2) the pangolin aspects, and finally (3) the cleavage site impart to SARS Cov-2?

    I gather from back-and-forth posts that the spike protein of SARS Cov-2 is derived from RATG13, but that within that spike protein are mutations yielding 5 or 6 amino acid changes to the S protein binding site that make the binding site itself closer to pangolin Cov 2020.

    Here's some of the back-and-forth conversation:

    The pangolin/1 has 5 out of 5 all-important RBD contact amino acids (AAs - red boxes) in common with the pangolin, and 8 out of 9 adjacent AAs (yellow boxes). It's closest 'bat relative' - RaTG13 only scores 1/5 for RBD contact, and 4/9 adjacent AAs. The other bat coronaviruses and SARS-classic are far worse.”

    ...The amino acid residues in question are L455, F486, Q493, S494,N501, and Y505. These six key positions within the Receptor Binding Domain portion of the Spike protein have been suggested to increase virulence as well as promote a firmer reception...

    ...More importantly, the Spike protein of RaTG13 scores 93.15% similarity to nCoV-2019 compared to only 84.52% from pCoV-MP789. The latter being the second higher scoring Spike comparison to this novel virus.

    Both the Spike protein (93.15/84.52) and the ORF1ab (96.52/90.36) are clear indicators that a Rhinopholus Affinis bat is the probable zoonotic origin of nCoV-2019

    We should consider the potency of the the RaTG13 spike protein as more significant than pCoV-MP789 while simultaneously accepting the 6 amino acid residues within the RBD of pCoV-MP789 provide higher virulency. Does this make sense? Both have their merits and nCoV-2019 appears to be a blend of the two.

    Finally,

    1. Why is Bat SARS Cov RAGT13 so significant? Where does it come from?

    2. Is the main significance of pangolin RNA the spike protein mutation features of SARS Cov-2 or are there other aspects of pangolin RNA in SARS Cov-2?

    3. Is the cleavage site unique?  I gather it is unrelated to either the bat or the pangolin RNA sources or to any other pertinent beta  corona virus in the B lineage?

    4. Is the cleavage site you refer to the furin cleavage site somewhere in the S1/S2 subunits of the spike protein of that facilitate viral entry and make it more virulent? Or is the another cleavage site thatis pertinent?

    5. Is this unique site cleaved by Cathepsin-L?

    4. Finally is this unique cleavage site the SUPERMAN feature that you refer to below:

    The KEY takeaway is that nCoV-2019 has a unique RNA insertion at a VERY crucial position that plays a vital role. That "type" of mutation is absent in ALL other betacovs (except one but lets ignore that lol).

    nCoV-2019 has this 1 specific SUPERMAN feature that no other betacoronavirus possesses; including the aforementioned Bat and Pangolin viruses.

    Thanks Dr. Mayer.

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  • Mon, Aug 03, 2020 - 8:58am

    #85
    Island girl

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    Innate immunity, herd immunity and vaccines

    Article from CNN describes research on T cell recognition of SARS-COv-2 in blood samples from people unexposed to this virus.  Some people show cross-reactivity, various possible implications.  I will also appended references from the primary literature.

    Easy to read article:

    https://www.cnn.com/2020/08/02/health/gupta-coronavirus-t-cell-cross-reactivity-immunity-wellness/index.html

    Some of the related research on T cell targets in those exposed and unexposed:

    https://www.cell.com/cell/pdf/S0092-8674(20)30610-3.pdf

    A review of knowns and unknowns by the researchers:

    https://www.nature.com/articles/s41577-020-0389-z

     

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