Smoking Gun: NIH Was Funding Research In China Into Producing Highly Transmissible Corona Virus Infectious To Humans

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in humans is selected for it's capacity to infect more human, which does me ans that when you run into one that has infected a lot of humans, it's goin g to look optimised for the job.

nows what they are talking about - that it's had the benefit of intelligent design by humans?

inion doesn't count.

le fiasco since day one. His ignorance and errors are too numerous to list.

t illustrate that he doesn't know what he is talking about.

does, but is clearly conserved by the fact that any significant change sto ps it working and kills off that strain of the virus. One can follow his th inking, but the fact that he can't see that he went wrong in very revealing way means that his opinion really can't be taken seriously.

escription of the spike protein.

One has to wonder why Fred included that. I was high-lighting the fact that he'd confused "conserved" with "not mutating", and nothing in this post ad dresses that bizarre oversight.

complishing something, have narrowed their focus on the ACE-2 receptor bind ing domain (RBD) of the spike protein.

Of course they would. That's the bit that does the work.

e to identify and observe antibodies produced for one virus working on the other.

That was one of the things that the "sychophantic" PNAS news article was ta lking about. The vaccine that was being developed against SARS is also acti ve against Covid-19, although the antigen being synthesised should be tweak ed to make the antibody evoked one that was slightly more active against Co vid-19.

tein of both SARS-CoV-1 and SARS-CoV-2, despite a genetic overlap of just 7

The overlap is over the whole 33k length of genome. The interesting questio n would be the matching between the segment - gene - that coded for the spi ke protein, and again - as you point out - the receptor binding segment of the spike protein would be crucial. The rest of the protein still has to fo ld into the right shape to put the receptor binding segment in the right pl ace at the right angle to work for the virus.

The CR3022 antibody is referred to in a 2006 paper

It was harvested from a patient who had recovered from SARS so it doesn't s eem to be what the PNAS news article was taking about.

The wet market was implicated in an outbreak of a new and nasty virus disea se. About half the early cases were associated with the market. It got ster ilised as a public health measure - the Chinese aren't nuts. Imagining that they were "covering up" anything is lunatic comnspiracy theory

The ancestral virus is found in bat that live 1000 miles away, and can't in fect humans. It seems likely that the more immediate ancestor of the Covid-

But much less likely to let a virus escape.

harvested bat virus for study.

Which would only infect bats.

It has elements that are similar to elements in HIV. They got into HIV natu rally, and could have got into Covid-19 equally naturally.

The grand-standing elderly Nobel Prize winner who got his Nobel Prize for w ork on the HIV virus is going to see more similarity to HIV than people wit h other interests.

After the SARS outbreak they were aware of the risks. Their actions don't l ook suspicious to rational people, but lots of irrational people are weighi ng in with some remarkably silly speculations.

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p in humans is selected for it's capacity to infect more human, which does means that when you run into one that has infected a lot of humans, it's go ing to look optimised for the job.

knows what they are talking about - that it's had the benefit of intellige nt design by humans?

opinion doesn't count.

hole fiasco since day one. His ignorance and errors are too numerous to lis t.

hat illustrate that he doesn't know what he is talking about.

it does, but is clearly conserved by the fact that any significant change s tops it working and kills off that strain of the virus. One can follow his thinking, but the fact that he can't see that he went wrong in very reveali ng way means that his opinion really can't be taken seriously.

description of the spike protein.

at he'd confused "conserved" with "not mutating", and nothing in this post addresses that bizarre oversight.

accomplishing something, have narrowed their focus on the ACE-2 receptor bi nding domain (RBD) of the spike protein.

ble to identify and observe antibodies produced for one virus working on th e other.

talking about. The vaccine that was being developed against SARS is also ac tive against Covid-19, although the antigen being synthesised should be twe aked to make the antibody evoked one that was slightly more active against Covid-19.

rotein of both SARS-CoV-1 and SARS-CoV-2, despite a genetic overlap of just 79% between the two viruses.

ion would be the matching between the segment - gene - that coded for the s pike protein, and again - as you point out - the receptor binding segment o f the spike protein would be crucial. The rest of the protein still has to fold into the right shape to put the receptor binding segment in the right place at the right angle to work for the virus.

seem to be what the PNAS news article was taking about.

If the RBD folds correctly for binding to ACE-2 then it will fold correctly for the antibody.

This is all good news for vaccines offering immunity not only across near m utations being observed but also across many strains.

It is probably bad news for developing fast antibody testing with any kind of specificity performance that would be useful for purposes of mitigation. This is why Birx recently announced we need a new antibody testing technol ogy.

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up in humans is selected for it's capacity to infect more human, which doe s means that when you run into one that has infected a lot of humans, it's going to look optimised for the job.

ho knows what they are talking about - that it's had the benefit of intelli gent design by humans?

i opinion doesn't count.

whole fiasco since day one. His ignorance and errors are too numerous to l ist.

that illustrate that he doesn't know what he is talking about.

n it does, but is clearly conserved by the fact that any significant change stops it working and kills off that strain of the virus. One can follow hi s thinking, but the fact that he can't see that he went wrong in very revea ling way means that his opinion really can't be taken seriously.

al description of the spike protein.

that he'd confused "conserved" with "not mutating", and nothing in this pos t addresses that bizarre oversight.

y accomplishing something, have narrowed their focus on the ACE-2 receptor binding domain (RBD) of the spike protein.

able to identify and observe antibodies produced for one virus working on the other.

s talking about. The vaccine that was being developed against SARS is also active against Covid-19, although the antigen being synthesised should be t weaked to make the antibody evoked one that was slightly more active agains t Covid-19.

protein of both SARS-CoV-1 and SARS-CoV-2, despite a genetic overlap of ju st 79% between the two viruses.

stion would be the matching between the segment - gene - that coded for the spike protein, and again - as you point out - the receptor binding segment of the spike protein would be crucial. The rest of the protein still has t o fold into the right shape to put the receptor binding segment in the righ t place at the right angle to work for the virus.

't seem to be what the PNAS news article was taking about.

ly for the antibody.

This does depend on what the antibody is looking for.

mutations being observed but also across many strains.

Perhaps.

d of specificity performance that would be useful for purposes of mitigatio n. This is why Birx recently announced we need a new antibody testing techn ology.

This assumes that we know the feature on the virus that the antibody is loo king for.

"?That really killed RSV vaccines for a generation,?says Pe ter Hotez, a vaccine researcher and dean of the National School of Tropical Medicine at Baylor College of Medicine in Houston, TX. After more than 50 years of further study, a candidate RSV vaccine is finally back in clinical trials.When SARS, also a corona virus, appeared in China and spread global ly nearly two decades ago, Hotez was among researchers who began investigat ing a potential vaccine. In early tests of his candidate, he witnessed how immune cells of vaccinated animals attacked lung tissue, in much the same w ay that the RSV vaccine had resulted in immune cells attacking kids? ? lungs.?I thought,?Oh crap,??he recalls, noting his initial fear that a safe vaccine may again not be possible. But his team revised their approach. Instead of producing the whole spike prot ein of the virus, they built just a tiny piece of it?the piece that attaches to human cells, called the receptor-binding domain."

Peter Hotez was talking about a rather specific way of persuading the body to produce a very specific antibody to just the receptor-binding domain.

Your CR3022 antibody was taken from the blood of a SARS patient. If the pap er spells out what it is targeting it's buried much to deep for me to dig d own to.

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and flu

ction.

ow up in humans is selected for it's capacity to infect more human, which d oes means that when you run into one that has infected a lot of humans, it' s going to look optimised for the job.

who knows what they are talking about - that it's had the benefit of intel ligent design by humans?

hi opinion doesn't count.

is whole fiasco since day one. His ignorance and errors are too numerous to list.

ms that illustrate that he doesn't know what he is talking about.

hen it does, but is clearly conserved by the fact that any significant chan ge stops it working and kills off that strain of the virus. One can follow his thinking, but the fact that he can't see that he went wrong in very rev ealing way means that his opinion really can't be taken seriously.

eral description of the spike protein.

t that he'd confused "conserved" with "not mutating", and nothing in this p ost addresses that bizarre oversight.

lly accomplishing something, have narrowed their focus on the ACE-2 recepto r binding domain (RBD) of the spike protein.

re able to identify and observe antibodies produced for one virus working o n the other.

was talking about. The vaccine that was being developed against SARS is als o active against Covid-19, although the antigen being synthesised should be tweaked to make the antibody evoked one that was slightly more active agai nst Covid-19.

ke protein of both SARS-CoV-1 and SARS-CoV-2, despite a genetic overlap of just 79% between the two viruses.

uestion would be the matching between the segment - gene - that coded for t he spike protein, and again - as you point out - the receptor binding segme nt of the spike protein would be crucial. The rest of the protein still has to fold into the right shape to put the receptor binding segment in the ri ght place at the right angle to work for the virus.

sn't seem to be what the PNAS news article was taking about.

ctly for the antibody.

ar mutations being observed but also across many strains.

ind of specificity performance that would be useful for purposes of mitigat ion. This is why Birx recently announced we need a new antibody testing tec hnology.

ooking for.

I don't see any work into distingusihing antibodies for the different strai ns of the virus thus far.

Peter Hotez, a vaccine researcher and dean of the National School of Tropic al Medicine at Baylor College of Medicine in Houston, TX. After more than 5

y to produce a very specific antibody to just the receptor-binding domain.

aper spells out what it is targeting it's buried much to deep for me to dig down to.

That's a snap these days with the mRNA vaccines in which they can use the g enetic sequence specifically coding for the RBD of the spike protein. Did you ask yourself what's going to happen when the body develops immunity to the viral vector of such vaccines? Didn't think so.

Have you looked into any other sources of the disease that might have been in the market?

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ds and flu

fection.

show up in humans is selected for it's capacity to infect more human, which does means that when you run into one that has infected a lot of humans, i t's going to look optimised for the job.

dy who knows what they are talking about - that it's had the benefit of int elligent design by humans?

so hi opinion doesn't count.

this whole fiasco since day one. His ignorance and errors are too numerous to list.

aims that illustrate that he doesn't know what he is talking about.

when it does, but is clearly conserved by the fact that any significant ch ange stops it working and kills off that strain of the virus. One can follo w his thinking, but the fact that he can't see that he went wrong in very r evealing way means that his opinion really can't be taken seriously.

eneral description of the spike protein.

act that he'd confused "conserved" with "not mutating", and nothing in this post addresses that bizarre oversight.

ually accomplishing something, have narrowed their focus on the ACE-2 recep tor binding domain (RBD) of the spike protein.

were able to identify and observe antibodies produced for one virus working on the other.

e was talking about. The vaccine that was being developed against SARS is a lso active against Covid-19, although the antigen being synthesised should be tweaked to make the antibody evoked one that was slightly more active ag ainst Covid-19.

pike protein of both SARS-CoV-1 and SARS-CoV-2, despite a genetic overlap o f just 79% between the two viruses.

question would be the matching between the segment - gene - that coded for the spike protein, and again - as you point out - the receptor binding seg ment of the spike protein would be crucial. The rest of the protein still h as to fold into the right shape to put the receptor binding segment in the right place at the right angle to work for the virus.

oesn't seem to be what the PNAS news article was taking about.

rectly for the antibody.

near mutations being observed but also across many strains.

kind of specificity performance that would be useful for purposes of mitig ation. This is why Birx recently announced we need a new antibody testing t echnology.

looking for.

ains of the virus thus far.

s Peter Hotez, a vaccine researcher and dean of the National School of Trop ical Medicine at Baylor College of Medicine in Houston, TX. After more than 50 years of further study, a candidate RSV vaccine is finally back in clin ical trials.When SARS, also a corona virus, appeared in China and spread gl obally nearly two decades ago, Hotez was among researchers who began invest igating a potential vaccine. In early tests of his candidate, he witnessed how immune cells of vaccinated animals attacked lung tissue, in much the sa me way that the RSV vaccine had resulted in immune cells attacking kids? ?? lungs.?I thought,?Oh crap,??he recal ls, noting his initial fear that a safe vaccine may again not be possible. But his team revised their approach. Instead of producing the whole spike p rotein of the virus, they built just a tiny piece of it?the piece t hat attaches to human cells, called the receptor-binding domain."

ody to produce a very specific antibody to just the receptor-binding domain .

paper spells out what it is targeting it's buried much to deep for me to d ig down to.

genetic sequence specifically coding for the RBD of the spike protein.

ty to the viral vector of such vaccines? Didn't think so.

Lunatics like you probably think that because the ACE-2 receptor the corona virus targets is designed to respond to a blood-pressure regulating protei n

the antibody is going to lock onto the same protein. This doesn't follow. T he receptor-binding-domain can lock onto the ACE2 receptor without being a close match to ACE-2 enzyme - only the bit that locks on has to match the r eceptor - and if it were a problem it wouldn't be difficult to stretch the receptor binding domain in a way that made the antibody that recogised it l ess likely to go after the ACE-2 enzyme.

This is a fairly obvious problem, with an equally obvious solution, obvious to those skilled in the art, and even to me (who isn't).

You learned how to weponize anthrax, and were able to avoid sharing that with foreigners. Maybe viruses are different to bacteria.

ed the

ews. It also explains why China was concentrating on shutting down Wuhan. I t was because that's where the lab escape occurred and they KNEW they had a REALLY BAD problem with that thing getting loose. Otherwise thy could care less about a corona virus epidemic, because, up until then, corona virus w as harmless. But for this one, they seemed to know beforehand it was anythi ng but harmless.

SARS? Hello? China had experience with SARS, H1N1, etc, to draw from. They locked down and controlled SARS, which was far deadlier than Covid.

It's certainly possible that the Wuhan lab was the source, but good luck finding evidence. That would require an international investigation and China isn't going to allow it.

n making a real doozy.

ngerous in 2014.

the National of Institutes of Health instituted a moratorium on the work, s uspending 21 studies."

advice as usual, resumed funding for the research in 2017:

d the moratorium and the second phase of the NIAID project, which included the gain-of-function research, began."

currence.

ones.

The gain of function scientists, around the world, believed that research was contributing to that. There has been disagreement and the opponents are probably right, but it is hotly debated in the science community.

It doesn't have to be "intelligent design" by humans. Gain of function started with and includes experiments whereby infection is moved through species in the lab, to see what happens, to see how the virus mutates and gains function, not with a specific design motive, though that research has also been going on.

That is by far the most logical, well thought post I've ever seen you make.

From what I see, it's not clear if bats were sold or not. It's also theorized that it could have come from Pangolins, which apparently were sold there. And even if the actual animal wasn't sold there, it's certainly possible that a vendor, people who worked there, people who shopped there, might have been involved with bats elsewhere and brought the virus there.

and

Seems the alternate, perfectly reasonable explanation for that is that they had a deadly virus on the loose and they knew the market was at least one area that was highly infected, regardless of where it came from. Like right now in the US we're busy disinfecting meat packing plants, because high number of employees are infected.

About 8 miles away or so.

No one is sure where it came from at this point, but it's true that bats are a leading suspect and the lab was harvesting bat virus and doing gain of function studies.

I've heard exactly the opposite, virologist saying that it shows no signs of what you'd expect you'd see with a genetically engineered virus.

I don't see anything suspicious in what they did afterwards, compared to other outbreaks. China has a history of covering up, minimizing, lie, etc.

ease. About half the early cases were associated with the market. It got st erilised as a public health measure - the Chinese aren't nuts. Imagining th at they were "covering up" anything is lunatic comnspiracy theory

infect humans. It seems likely that the more immediate ancestor of the Covi d-19 virus had made the jump to some other species before it made the next step to humans. Pangolins are a possible intermediate host. They couldn't h ave been legally sold at the Wuhan wet market, but some illegal trade doe s seem to have gone on.

ad harvested bat virus for study.

BS. Read up on "gain of function" research. That is what the Wuhan lab was doing. Hint: the function gained is the ability to transmit to other species, to become more effective at transmission, etc.

turally, and could have got into Covid-19 equally naturally.

work on the HIV virus is going to see more similarity to HIV than people w ith other interests.

look suspicious to rational people, but lots of irrational people are weig hing in with some remarkably silly speculations.

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olds and flu

infection.

t show up in humans is selected for it's capacity to infect more human, whi ch does means that when you run into one that has infected a lot of humans, it's going to look optimised for the job.

body who knows what they are talking about - that it's had the benefit of i ntelligent design by humans?

, so hi opinion doesn't count.

f this whole fiasco since day one. His ignorance and errors are too numerou s to list.

claims that illustrate that he doesn't know what he is talking about.

- when it does, but is clearly conserved by the fact that any significant change stops it working and kills off that strain of the virus. One can fol low his thinking, but the fact that he can't see that he went wrong in very revealing way means that his opinion really can't be taken seriously.

general description of the spike protein.

fact that he'd confused "conserved" with "not mutating", and nothing in th is post addresses that bizarre oversight.

ctually accomplishing something, have narrowed their focus on the ACE-2 rec eptor binding domain (RBD) of the spike protein.

y were able to identify and observe antibodies produced for one virus worki ng on the other.

cle was talking about. The vaccine that was being developed against SARS is also active against Covid-19, although the antigen being synthesised shoul d be tweaked to make the antibody evoked one that was slightly more active against Covid-19.

spike protein of both SARS-CoV-1 and SARS-CoV-2, despite a genetic overlap of just 79% between the two viruses.

ng question would be the matching between the segment - gene - that coded f or the spike protein, and again - as you point out - the receptor binding s egment of the spike protein would be crucial. The rest of the protein still has to fold into the right shape to put the receptor binding segment in th e right place at the right angle to work for the virus.

doesn't seem to be what the PNAS news article was taking about.

orrectly for the antibody.

s near mutations being observed but also across many strains.

ny kind of specificity performance that would be useful for purposes of mit igation. This is why Birx recently announced we need a new antibody testing technology.

is looking for.

trains of the virus thus far.

ays Peter Hotez, a vaccine researcher and dean of the National School of Tr opical Medicine at Baylor College of Medicine in Houston, TX. After more th an 50 years of further study, a candidate RSV vaccine is finally back in cl inical trials.When SARS, also a corona virus, appeared in China and spread globally nearly two decades ago, Hotez was among researchers who began inve stigating a potential vaccine. In early tests of his candidate, he witnesse d how immune cells of vaccinated animals attacked lung tissue, in much the same way that the RSV vaccine had resulted in immune cells attacking kids ? lungs.?I thought,?Oh crap,??he re calls, noting his initial fear that a safe vaccine may again not be possibl e. But his team revised their approach. Instead of producing the whole spik e protein of the virus, they built just a tiny piece of it?the piec e that attaches to human cells, called the receptor-binding domain."

body to produce a very specific antibody to just the receptor-binding doma in.

he paper spells out what it is targeting it's buried much to deep for me to dig down to.

he genetic sequence specifically coding for the RBD of the spike protein.

nity to the viral vector of such vaccines? Didn't think so.

na virus targets is designed to respond to a blood-pressure regulating prot ein

This is your standrad ploy of spouting even more idiotic gibberish to get o ut from under your previous idiotic gibberish.

The receptor-binding-domain can lock onto the ACE2 receptor without being a close match to ACE-2 enzyme - only the bit that locks on has to match the receptor - and if it were a problem it wouldn't be difficult to stretch th e receptor binding domain in a way that made the antibody that recogised it less likely to go after the ACE-2 enzyme.

us to those skilled in the art, and even to me (who isn't).

You missed the point entirely. The immunity I was talking about was the for the viral vector whose job it is to infect cells and incorporate its DNA i nto the nucleus for the purpose of producing antiviral antigens. Care to ex plain how that's going to happen if the immune system is catching these vec tors before they have a chance to infect cells, or killing infecting cells before they have a chance to produce antigen?

Nature does more genetic experiments every second than humans can do in 1000 years. The most likely path of C19 is that some researcher crawled into a cave somewhere, deliberately collected bat virus samples, transported them to the lab in wuhan, and it got loose from there.

Ricky C wrote in news: snipped-for-privacy@googlegroups.com:

He must have been whopped upside da haed with the same composure plank that Donald John Trump got hit with the other day when he only jumped on one reporter at the very end of the meeting. He was calm the whole meeting. Whatever they beat him with, I hope they beat him to death with it. (either or both)(Trump and HooTard)

You do understand there are drugs that can accelerate randomization of viral DNA and mutation rate? The principle is actually the basis for a brand new antiviral cure that just received emergency approval to enter human trials.

This is not a new concept, it's been around for over 20 years that I know of.

ote:

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the genetic sequence specifically coding for the RBD of the spike protein.

munity to the viral vector of such vaccines? Didn't think so.

rona virus targets is designed to respond to a blood-pressure regulating pr otein

out from under your previous idiotic gibberish.

You do take the attitude that anybody who doesn't accept your particular li ne of half-baked idiotic gibberish is spouting idiotic gibberish.

The fact that you can't understand it doesn't automatically make it idiotic gibberish, much as you might like that to be true.

w. The receptor-binding-domain can lock onto the ACE2 receptor without bein g a close match to ACE-2 enzyme - only the bit that locks on has to match t he receptor - and if it were a problem it wouldn't be difficult to stretch the receptor binding domain in a way that made the antibody that recogised it less likely to go after the ACE-2 enzyme.

ious to those skilled in the art, and even to me (who isn't).

or the viral vector whose job it is to infect cells and incorporate its DNA into the nucleus for the purpose of producing antiviral antigens. Care to explain how that's going to happen if the immune system is catching these v ectors before they have a chance to infect cells, or killing infecting cell s before they have a chance to produce antigen?

Easy. The viral vector isn't a corona virus. Corona viruses have an RNA cor e, for a start.

" A virus such as measles or adenovirus is genetically engineered so that i t can produce coronavirus proteins in the body."

Next - equally idiotic - question?

Note that I'm able to find and post links to published research that backs up what I have to say. You don't seem to be able to manage that, and when y ou try you turn out to have misunderstood what you thought supported your c laim.