Smoking Gun: NIH Was Funding Research In China Into Producin

bloggs.fredbloggs.fred@gmail.com wrote in news:3b1e86a5-4416-43eb-ba69-
13eb138552c9@googlegroups.com:

> See antibody CR3022

We can kill it with a watch battery?

It would make a nice Trump joke except he is way too stupid to know
what a watch battery is / looks like / is called.

 

[Tom Del Rosso]

Ricky C wrote:

On Wednesday, April 29, 2020 at 10:36:18 PM UTC-4, Tom Del Rosso
wrote:
John Larkin wrote:

There's no nationalistic advantage to researching viruses. Whatever
we learn will be shared with the world.

We would but China wouldn't. Some in this thread have said that the
Trump administration restarted the research, but actually it was a
Chinese scientist who went back to China and resumed it. They
obviously created it a lab and had an accident.

Why is that "obvious"? I've seen no reasonable evidence to support
that idea, much less compelling evidence.

They claimed it came from the market, but bats weren't sold there, and
they sterilized the place before samples of the original strain could be
taken. So they were covering up the fact that it wasn't there.

The lab is near the market.

It come from bats that live 1000 miles away, and they had harvested bat
virus for study.

It has elements of HIV that are not likely to get in it naturally.

Because of this and some other bits and pieces, their actions were
suspicious in ways not consistent with what they did after past
outbreaks.

 

[Bill Sloman]

On Thursday, April 30, 2020 at 9:04:42 PM UTC+10, bloggs.fre...@gmail.com wrote:

On Wednesday, April 29, 2020 at 9:00:03 PM UTC-4, Bill Sloman wrote:
On Thursday, April 30, 2020 at 10:24:35 AM UTC+10, bloggs.fre...@gmail.com wrote:
On Wednesday, April 29, 2020 at 7:22:13 PM UTC-4, Bill Sloman wrote:
On Thursday, April 30, 2020 at 1:50:47 AM UTC+10, bloggs.fre...@gmail.com wrote:
On Wednesday, April 29, 2020 at 11:27:11 AM UTC-4, jla...@highlandsniptechnology.com wrote:
On Wed, 29 Apr 2020 07:49:09 -0700 (PDT),
bloggs.fredbloggs.fred@gmail.com wrote:

On Wednesday, April 29, 2020 at 10:38:21 AM UTC-4, jla...@highlandsniptechnology.com wrote:
On Wed, 29 Apr 2020 05:25:30 -0700 (PDT),
bloggs.fredbloggs.fred@gmail.com wrote:

snip

C19 could be natural. All the previous centuries of colds and flu
were. We get colds and flu every winter.

Not likely to be natural, it's too optimized for human infection.

Natural selection is perfectly natural, and any virus that 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, it's going to look optimised for the job.

What's special about Covid-19 that has suggested - to anybody who knows what they are talking about - that it's had the benefit of intelligent design by humans?

Fred Bloggs clearly doesn't know what he is talking about, so hi opinion doesn't count.

So says Sloman who has been wrong about every last aspect of this whole fiasco since day one. His ignorance and errors are too numerous to list.

Whereas I have cited a few points where Fred Bloggs has made claims that illustrate that he doesn't know what he is talking about.

He claimed that the corona virus spike protein doesn't mutate - 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 follow 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.

snipped Fred being even more stupid than usual

Once again you couldn't be more wrong. No one cares about any general description 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 addresses that bizarre oversight.

> The people who actually work with this virus, with the aim of actually accomplishing something, have narrowed their focus on the ACE-2 receptor binding domain (RBD) of the spike protein.

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

> They find the RBD to be "highly conserved," so much so that they were able 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 talking about. The vaccine that was being developed against SARS is also active against Covid-19, although the antigen being synthesised should be tweaked to make the antibody evoked one that was slightly more active against Covid-19.

https://www.pnas.org/content/pnas/117/15/8218.full.pdf

> See antibody CR3022 as one example of an antibody targeting the spike protein of both SARS-CoV-1 and SARS-CoV-2, despite a genetic overlap of just 79% between the two viruses.

The overlap is over the whole 33k length of genome. The interesting question 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 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.

The CR3022 antibody is referred to in a 2006 paper

https://www.ncbi.nlm.nih.gov/pubmed/16796401

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


--
Bill Sloman, Sydney

 

[Bill Sloman]

On Thursday, April 30, 2020 at 10:47:56 PM UTC+10, Tom Del Rosso wrote:

Ricky C wrote:
On Wednesday, April 29, 2020 at 10:36:18 PM UTC-4, Tom Del Rosso
wrote:
John Larkin wrote:

There's no nationalistic advantage to researching viruses. Whatever
we learn will be shared with the world.

We would but China wouldn't. Some in this thread have said that the
Trump administration restarted the research, but actually it was a
Chinese scientist who went back to China and resumed it. They
obviously created it a lab and had an accident.

Why is that "obvious"? I've seen no reasonable evidence to support
that idea, much less compelling evidence.

They claimed it came from the market, but bats weren't sold there, and
they sterilized the place before samples of the original strain could be
taken. So they were covering up the fact that it wasn't there.

The wet market was implicated in an outbreak of a new and nasty virus disease. About half the early cases were associated with the market. It got sterilised 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 infect humans. It seems likely that the more immediate ancestor of the Covid-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 have been legally sold at the Wuhan wet market, but some illegal trade does seem to have gone on.

> The lab is near the market.

But much less likely to let a virus escape.

> It come from bats that live 1000 miles away - not directly - and they had harvested bat virus for study.

Which would only infect bats.

> It has elements of HIV that are not likely to get in it naturally.

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

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

Because of this and some other bits and pieces, their actions were
suspicious in ways not consistent with what they did after past
outbreaks.

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

--
Bill Sloman, Sydney

 

On Thursday, April 30, 2020 at 9:25:12 AM UTC-4, Bill Sloman wrote:

On Thursday, April 30, 2020 at 9:04:42 PM UTC+10, bloggs.fre...@gmail.com wrote:
On Wednesday, April 29, 2020 at 9:00:03 PM UTC-4, Bill Sloman wrote:
On Thursday, April 30, 2020 at 10:24:35 AM UTC+10, bloggs.fre...@gmail.com wrote:
On Wednesday, April 29, 2020 at 7:22:13 PM UTC-4, Bill Sloman wrote:
On Thursday, April 30, 2020 at 1:50:47 AM UTC+10, bloggs.fre...@gmail.com wrote:
On Wednesday, April 29, 2020 at 11:27:11 AM UTC-4, jla...@highlandsniptechnology.com wrote:
On Wed, 29 Apr 2020 07:49:09 -0700 (PDT),
bloggs.fredbloggs.fred@gmail.com wrote:

On Wednesday, April 29, 2020 at 10:38:21 AM UTC-4, jla...@highlandsniptechnology.com wrote:
On Wed, 29 Apr 2020 05:25:30 -0700 (PDT),
bloggs.fredbloggs.fred@gmail.com wrote:

snip

C19 could be natural. All the previous centuries of colds and flu
were. We get colds and flu every winter.

Not likely to be natural, it's too optimized for human infection.

Natural selection is perfectly natural, and any virus that 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, it's going to look optimised for the job.

What's special about Covid-19 that has suggested - to anybody who knows what they are talking about - that it's had the benefit of intelligent design by humans?

Fred Bloggs clearly doesn't know what he is talking about, so hi opinion doesn't count.

So says Sloman who has been wrong about every last aspect of this whole fiasco since day one. His ignorance and errors are too numerous to list.

Whereas I have cited a few points where Fred Bloggs has made claims that illustrate that he doesn't know what he is talking about.

He claimed that the corona virus spike protein doesn't mutate - 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 follow 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.

snipped Fred being even more stupid than usual

Once again you couldn't be more wrong. No one cares about any general description 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 addresses that bizarre oversight.

The people who actually work with this virus, with the aim of actually accomplishing something, have narrowed their focus on the ACE-2 receptor binding domain (RBD) of the spike protein.

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

They find the RBD to be "highly conserved," so much so that they were able 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 talking about. The vaccine that was being developed against SARS is also active against Covid-19, although the antigen being synthesised should be tweaked to make the antibody evoked one that was slightly more active against Covid-19.

https://www.pnas.org/content/pnas/117/15/8218.full.pdf

See antibody CR3022 as one example of an antibody targeting the spike protein of both SARS-CoV-1 and SARS-CoV-2, despite a genetic overlap of just 79% between the two viruses.

The overlap is over the whole 33k length of genome. The interesting question 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 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.

The CR3022 antibody is referred to in a 2006 paper

https://www.ncbi.nlm.nih.gov/pubmed/16796401

It was harvested from a patient who had recovered from SARS so it doesn't 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 mutations 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 technology.

--
Bill Sloman, Sydney

 

[Bill Sloman]

On Friday, May 1, 2020 at 12:03:47 AM UTC+10, bloggs.fre...@gmail.com wrote:

On Thursday, April 30, 2020 at 9:25:12 AM UTC-4, Bill Sloman wrote:
On Thursday, April 30, 2020 at 9:04:42 PM UTC+10, bloggs.fre...@gmail.com wrote:
On Wednesday, April 29, 2020 at 9:00:03 PM UTC-4, Bill Sloman wrote:
On Thursday, April 30, 2020 at 10:24:35 AM UTC+10, bloggs.fre...@gmail.com wrote:
On Wednesday, April 29, 2020 at 7:22:13 PM UTC-4, Bill Sloman wrote:
On Thursday, April 30, 2020 at 1:50:47 AM UTC+10, bloggs.fre...@gmail.com wrote:
On Wednesday, April 29, 2020 at 11:27:11 AM UTC-4, jla...@highlandsniptechnology.com wrote:
On Wed, 29 Apr 2020 07:49:09 -0700 (PDT),
bloggs.fredbloggs.fred@gmail.com wrote:

On Wednesday, April 29, 2020 at 10:38:21 AM UTC-4, jla...@highlandsniptechnology.com wrote:
On Wed, 29 Apr 2020 05:25:30 -0700 (PDT),
bloggs.fredbloggs.fred@gmail.com wrote:

snip

C19 could be natural. All the previous centuries of colds and flu
were. We get colds and flu every winter.

Not likely to be natural, it's too optimized for human infection.

Natural selection is perfectly natural, and any virus that 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, it's going to look optimised for the job.

What's special about Covid-19 that has suggested - to anybody who knows what they are talking about - that it's had the benefit of intelligent design by humans?

Fred Bloggs clearly doesn't know what he is talking about, so hi opinion doesn't count.

So says Sloman who has been wrong about every last aspect of this whole fiasco since day one. His ignorance and errors are too numerous to list.

Whereas I have cited a few points where Fred Bloggs has made claims that illustrate that he doesn't know what he is talking about.

He claimed that the corona virus spike protein doesn't mutate - 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 follow 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.

snipped Fred being even more stupid than usual

Once again you couldn't be more wrong. No one cares about any general description 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 addresses that bizarre oversight.

The people who actually work with this virus, with the aim of actually accomplishing something, have narrowed their focus on the ACE-2 receptor binding domain (RBD) of the spike protein.

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

They find the RBD to be "highly conserved," so much so that they were able 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 talking about. The vaccine that was being developed against SARS is also active against Covid-19, although the antigen being synthesised should be tweaked to make the antibody evoked one that was slightly more active against Covid-19.

https://www.pnas.org/content/pnas/117/15/8218.full.pdf

See antibody CR3022 as one example of an antibody targeting the spike protein of both SARS-CoV-1 and SARS-CoV-2, despite a genetic overlap of just 79% between the two viruses.

The overlap is over the whole 33k length of genome. The interesting question 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 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.

The CR3022 antibody is referred to in a 2006 paper

https://www.ncbi.nlm.nih.gov/pubmed/16796401

It was harvested from a patient who had recovered from SARS so it doesn't 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 does depend on what the antibody is looking for.

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

Perhaps.

> 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 technology.

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

https://www.pnas.org/content/pnas/117/15/8218.full.pdf

"“That really killed RSV vaccines for a generation,”says Peter 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 globally nearly two decades ago, Hotez was among researchers who began investigating a potential vaccine. In early tests of his candidate, he witnessed 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 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 protein 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 paper spells out what it is targeting it's buried much to deep for me to dig down to.

--
Bill Sloman, Sydney

 

On Thursday, April 30, 2020 at 10:59:13 AM UTC-4, Bill Sloman wrote:

On Friday, May 1, 2020 at 12:03:47 AM UTC+10, bloggs.fre...@gmail.com wrote:
On Thursday, April 30, 2020 at 9:25:12 AM UTC-4, Bill Sloman wrote:
On Thursday, April 30, 2020 at 9:04:42 PM UTC+10, bloggs.fre...@gmail..com wrote:
On Wednesday, April 29, 2020 at 9:00:03 PM UTC-4, Bill Sloman wrote:
On Thursday, April 30, 2020 at 10:24:35 AM UTC+10, bloggs.fre...@gmail.com wrote:
On Wednesday, April 29, 2020 at 7:22:13 PM UTC-4, Bill Sloman wrote:
On Thursday, April 30, 2020 at 1:50:47 AM UTC+10, bloggs.fre....@gmail.com wrote:
On Wednesday, April 29, 2020 at 11:27:11 AM UTC-4, jla...@highlandsniptechnology.com wrote:
On Wed, 29 Apr 2020 07:49:09 -0700 (PDT),
bloggs.fredbloggs.fred@gmail.com wrote:

On Wednesday, April 29, 2020 at 10:38:21 AM UTC-4, jla....@highlandsniptechnology.com wrote:
On Wed, 29 Apr 2020 05:25:30 -0700 (PDT),
bloggs.fredbloggs.fred@gmail.com wrote:

snip

C19 could be natural. All the previous centuries of colds and flu
were. We get colds and flu every winter.

Not likely to be natural, it's too optimized for human infection.

Natural selection is perfectly natural, and any virus that 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, it's going to look optimised for the job.

What's special about Covid-19 that has suggested - to anybody who knows what they are talking about - that it's had the benefit of intelligent design by humans?

Fred Bloggs clearly doesn't know what he is talking about, so hi opinion doesn't count.

So says Sloman who has been wrong about every last aspect of this whole fiasco since day one. His ignorance and errors are too numerous to list.

Whereas I have cited a few points where Fred Bloggs has made claims that illustrate that he doesn't know what he is talking about.

He claimed that the corona virus spike protein doesn't mutate - 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 follow 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.

snipped Fred being even more stupid than usual

Once again you couldn't be more wrong. No one cares about any general description 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 addresses that bizarre oversight.

The people who actually work with this virus, with the aim of actually accomplishing something, have narrowed their focus on the ACE-2 receptor binding domain (RBD) of the spike protein.

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

They find the RBD to be "highly conserved," so much so that they were able 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 talking about. The vaccine that was being developed against SARS is also active against Covid-19, although the antigen being synthesised should be tweaked to make the antibody evoked one that was slightly more active against Covid-19.

https://www.pnas.org/content/pnas/117/15/8218.full.pdf

See antibody CR3022 as one example of an antibody targeting the spike protein of both SARS-CoV-1 and SARS-CoV-2, despite a genetic overlap of just 79% between the two viruses.

The overlap is over the whole 33k length of genome. The interesting question 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 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.

The CR3022 antibody is referred to in a 2006 paper

https://www.ncbi.nlm.nih.gov/pubmed/16796401

It was harvested from a patient who had recovered from SARS so it doesn't 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 does depend on what the antibody is looking for.

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

Perhaps.

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 technology.

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

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

https://www.pnas.org/content/pnas/117/15/8218.full.pdf

"“That really killed RSV vaccines for a generation,”says Peter 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 globally nearly two decades ago, Hotez was among researchers who began investigating a potential vaccine. In early tests of his candidate, he witnessed 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 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 protein 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 paper 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 genetic 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.

--
Bill Sloman, Sydney

 

[Ricky C]

On Thursday, April 30, 2020 at 8:47:56 AM UTC-4, Tom Del Rosso wrote:

Ricky C wrote:
On Wednesday, April 29, 2020 at 10:36:18 PM UTC-4, Tom Del Rosso
wrote:
John Larkin wrote:

There's no nationalistic advantage to researching viruses. Whatever
we learn will be shared with the world.

We would but China wouldn't. Some in this thread have said that the
Trump administration restarted the research, but actually it was a
Chinese scientist who went back to China and resumed it. They
obviously created it a lab and had an accident.

Why is that "obvious"? I've seen no reasonable evidence to support
that idea, much less compelling evidence.

They claimed it came from the market, but bats weren't sold there, and
they sterilized the place before samples of the original strain could be
taken. So they were covering up the fact that it wasn't there.

The lab is near the market.

It come from bats that live 1000 miles away, and they had harvested bat
virus for study.

It has elements of HIV that are not likely to get in it naturally.

Because of this and some other bits and pieces, their actions were
suspicious in ways not consistent with what they did after past
outbreaks.

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

--

Rick C.

+ Get 1,000 miles of free Supercharging
+ Tesla referral code - https://ts.la/richard11209

 

[Bill Sloman]

On Friday, May 1, 2020 at 3:13:09 AM UTC+10, bloggs.fre...@gmail.com wrote:

On Thursday, April 30, 2020 at 10:59:13 AM UTC-4, Bill Sloman wrote:
On Friday, May 1, 2020 at 12:03:47 AM UTC+10, bloggs.fre...@gmail.com wrote:
On Thursday, April 30, 2020 at 9:25:12 AM UTC-4, Bill Sloman wrote:
On Thursday, April 30, 2020 at 9:04:42 PM UTC+10, bloggs.fre...@gmail.com wrote:
On Wednesday, April 29, 2020 at 9:00:03 PM UTC-4, Bill Sloman wrote:
On Thursday, April 30, 2020 at 10:24:35 AM UTC+10, bloggs.fre....@gmail.com wrote:
On Wednesday, April 29, 2020 at 7:22:13 PM UTC-4, Bill Sloman wrote:
On Thursday, April 30, 2020 at 1:50:47 AM UTC+10, bloggs.fre...@gmail.com wrote:
On Wednesday, April 29, 2020 at 11:27:11 AM UTC-4, jla...@highlandsniptechnology.com wrote:
On Wed, 29 Apr 2020 07:49:09 -0700 (PDT),
bloggs.fredbloggs.fred@gmail.com wrote:

On Wednesday, April 29, 2020 at 10:38:21 AM UTC-4, jla....@highlandsniptechnology.com wrote:
On Wed, 29 Apr 2020 05:25:30 -0700 (PDT),
bloggs.fredbloggs.fred@gmail.com wrote:

snip

C19 could be natural. All the previous centuries of colds and flu
were. We get colds and flu every winter.

Not likely to be natural, it's too optimized for human infection.

Natural selection is perfectly natural, and any virus that 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, it's going to look optimised for the job.

What's special about Covid-19 that has suggested - to anybody who knows what they are talking about - that it's had the benefit of intelligent design by humans?

Fred Bloggs clearly doesn't know what he is talking about, so hi opinion doesn't count.

So says Sloman who has been wrong about every last aspect of this whole fiasco since day one. His ignorance and errors are too numerous to list.

Whereas I have cited a few points where Fred Bloggs has made claims that illustrate that he doesn't know what he is talking about.

He claimed that the corona virus spike protein doesn't mutate - 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 follow 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.

snipped Fred being even more stupid than usual

Once again you couldn't be more wrong. No one cares about any general description 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 addresses that bizarre oversight.

The people who actually work with this virus, with the aim of actually accomplishing something, have narrowed their focus on the ACE-2 receptor binding domain (RBD) of the spike protein.

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

They find the RBD to be "highly conserved," so much so that they were able 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 talking about. The vaccine that was being developed against SARS is also active against Covid-19, although the antigen being synthesised should be tweaked to make the antibody evoked one that was slightly more active against Covid-19.

https://www.pnas.org/content/pnas/117/15/8218.full.pdf

See antibody CR3022 as one example of an antibody targeting the spike protein of both SARS-CoV-1 and SARS-CoV-2, despite a genetic overlap of just 79% between the two viruses.

The overlap is over the whole 33k length of genome. The interesting question 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 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.

The CR3022 antibody is referred to in a 2006 paper

https://www.ncbi.nlm.nih.gov/pubmed/16796401

It was harvested from a patient who had recovered from SARS so it doesn't 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 does depend on what the antibody is looking for.

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

Perhaps.

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 technology.

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

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


https://www.pnas.org/content/pnas/117/15/8218.full.pdf

"“That really killed RSV vaccines for a generation,”says Peter 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 globally nearly two decades ago, Hotez was among researchers who began investigating a potential vaccine. In early tests of his candidate, he witnessed 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 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 protein 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 paper 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 genetic 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.

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

https://en.wikipedia.org/wiki/Angiotensin-converting_enzyme_2

the antibody is going to lock onto the same protein. This doesn't follow. 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 the receptor binding domain in a way that made the antibody that recogised it less 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).

--
Bill Sloman, Sydney

 

[Jasen Betts]

On 2020-04-29, John Larkin <jlarkin@highland_atwork_technology.com> wrote:

There's no nationalistic advantage to researching viruses. Whatever we
learn will be shared with the world.

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

--
Jasen.

 

[Whoey Louie]

On Wednesday, April 29, 2020 at 10:49:16 AM UTC-4, bloggs.fre...@gmail.com wrote:

On Wednesday, April 29, 2020 at 10:38:21 AM UTC-4, jla...@highlandsniptechnology.com wrote:
On Wed, 29 Apr 2020 05:25:30 -0700 (PDT),
bloggs.fredbloggs.fred@gmail.com wrote:

It's called gain-of-function research. And they apparently succeeded in making a real doozy.

The Obama administration halted funding for the research deemed too dangerous in 2014.

"Nevertheless, in 2014, under pressure from the Obama administration, the National of Institutes of Health instituted a moratorium on the work, suspending 21 studies."

Then the geniuses in the Trump administration, ignoring top scientific advice as usual, resumed funding for the research in 2017:

"Three years later, though擁n December 2017葉he NIH ended the moratorium and the second phase of the NIAID project, which included the gain-of-function research, began."

Coincidence? Only a fool would believe the SARS-Cov-2 was a natural occurrence.

https://www.newsweek.com/dr-fauci-backed-controversial-wuhan-lab-millions-us-dollars-risky-coronavirus-research-1500741?amp=1

What Republican administration do you blame for inventing the 1918 flu
virus?

NIH is supposed to be researching cures for disease, and not creating new 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.

--

John Larkin Highland Technology, Inc

Science teaches us to doubt.

Claude Bernard

 

[Whoey Louie]

On Wednesday, April 29, 2020 at 10:59:46 AM UTC-4, bloggs.fre...@gmail.com wrote:

On Wednesday, April 29, 2020 at 10:48:31 AM UTC-4, DecadentLinux...@decadence.org wrote:
jlarkin@highlandsniptechnology.com wrote in
news:cv3jaf9it3qggm1thmf3tpcn1o7p81da2k@4ax.com:

On Wed, 29 Apr 2020 05:25:30 -0700 (PDT),
bloggs.fredbloggs.fred@gmail.com wrote:

It's called gain-of-function research. And they apparently
succeeded in making a real doozy.

The Obama administration halted funding for the research deemed
too dangerous in 2014.

"Nevertheless, in 2014, under pressure from the Obama
administration, the National of Institutes of Health instituted a
moratorium on the work, suspending 21 studies."

Then the geniuses in the Trump administration, ignoring top
scientific advice as usual, resumed funding for the research in
2017:

"Three years later, though擁n December 2017葉he NIH ended the
moratorium and the second phase of the NIAID project, which
included the gain-of-function research, began."

Coincidence? Only a fool would believe the SARS-Cov-2 was a
natural occurrence.

https://www.newsweek.com/dr-fauci-backed-controversial-wuhan-lab-mi
llions-us-dollars-risky-coronavirus-research-1500741?amp=1

What Republican administration do you blame for inventing the 1918
flu virus?

The one that was in at the time, and the one just before that.

Bureaucracy growth was the rule of the day back then. Greedy
bastards as bad as Trump were rampant.

But inventing viruses? Usually outside a republican's mental and
intellectual purview. Definitely not outside their moral purview.

IOW, too stupid to do or come up with it, but definitely stupid
enough to concoct the idea and put it forth or even pay to have it
done.

But back then? They did not even know much about airborne
particulate at all.

You say some stupid shit though. Thought I would reference why.
The word for today is mindset.
Civil mindsets are different than careless idiot mindsets.

You hit number 2, Johnny.

Fauci knew what had happened in China before the outbreak even made the news. It also explains why China was concentrating on shutting down Wuhan. It 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 was harmless. But for this one, they seemed to know beforehand it was anything 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.

 

[Whoey Louie]

On Wednesday, April 29, 2020 at 7:22:13 PM UTC-4, Bill Sloman wrote:

On Thursday, April 30, 2020 at 1:50:47 AM UTC+10, bloggs.fre...@gmail.com wrote:
On Wednesday, April 29, 2020 at 11:27:11 AM UTC-4, jla...@highlandsniptechnology.com wrote:
On Wed, 29 Apr 2020 07:49:09 -0700 (PDT),
bloggs.fredbloggs.fred@gmail.com wrote:

On Wednesday, April 29, 2020 at 10:38:21 AM UTC-4, jla...@highlandsniptechnology.com wrote:
On Wed, 29 Apr 2020 05:25:30 -0700 (PDT),
bloggs.fredbloggs.fred@gmail.com wrote:

snip

C19 could be natural. All the previous centuries of colds and flu
were. We get colds and flu every winter.

Not likely to be natural, it's too optimized for human infection.

Natural selection is perfectly natural, and any virus that 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, it's going to look optimised for the job.

What's special about Covid-19 that has suggested - to anybody who knows what they are talking about - that it's had the benefit of intelligent design by humans?

Fred Bloggs clearly doesn't know what he is talking about, so hi opinion doesn't count.

--
Bill Sloman, Sydney

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.

 

[Ricky C]

On Friday, May 1, 2020 at 10:08:35 AM UTC-4, Whoey Louie wrote:

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.

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

--

Rick C.

-- Get 1,000 miles of free Supercharging
-- Tesla referral code - https://ts.la/richard11209

 

[Whoey Louie]

On Thursday, April 30, 2020 at 8:47:56 AM UTC-4, Tom Del Rosso wrote:

Ricky C wrote:
On Wednesday, April 29, 2020 at 10:36:18 PM UTC-4, Tom Del Rosso
wrote:
John Larkin wrote:

There's no nationalistic advantage to researching viruses. Whatever
we learn will be shared with the world.

We would but China wouldn't. Some in this thread have said that the
Trump administration restarted the research, but actually it was a
Chinese scientist who went back to China and resumed it. They
obviously created it a lab and had an accident.

Why is that "obvious"? I've seen no reasonable evidence to support
that idea, much less compelling evidence.

They claimed it came from the market, but bats weren't sold there,

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

they sterilized the place before samples of the original strain could be
taken. So they were covering up the fact that it wasn't there.

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.

The lab is near the market.

About 8 miles away or so.

It come from bats that live 1000 miles away, and they had harvested bat
virus for study.

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.

It has elements of HIV that are not likely to get in it naturally.

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.

Because of this and some other bits and pieces, their actions were
suspicious in ways not consistent with what they did after past
outbreaks.

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.

 

[Whoey Louie]

On Thursday, April 30, 2020 at 9:51:57 AM UTC-4, Bill Sloman wrote:

On Thursday, April 30, 2020 at 10:47:56 PM UTC+10, Tom Del Rosso wrote:
Ricky C wrote:
On Wednesday, April 29, 2020 at 10:36:18 PM UTC-4, Tom Del Rosso
wrote:
John Larkin wrote:

There's no nationalistic advantage to researching viruses. Whatever
we learn will be shared with the world.

We would but China wouldn't. Some in this thread have said that the
Trump administration restarted the research, but actually it was a
Chinese scientist who went back to China and resumed it. They
obviously created it a lab and had an accident.

Why is that "obvious"? I've seen no reasonable evidence to support
that idea, much less compelling evidence.

They claimed it came from the market, but bats weren't sold there, and
they sterilized the place before samples of the original strain could be
taken. So they were covering up the fact that it wasn't there.

The wet market was implicated in an outbreak of a new and nasty virus disease. About half the early cases were associated with the market. It got sterilised 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 infect humans. It seems likely that the more immediate ancestor of the Covid-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 have been legally sold at the Wuhan wet market, but some illegal trade does seem to have gone on.

The lab is near the market.

But much less likely to let a virus escape.

It come from bats that live 1000 miles away - not directly - and they had harvested bat virus for study.

Which would only infect bats.

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.

It has elements of HIV that are not likely to get in it naturally.

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

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

Because of this and some other bits and pieces, their actions were
suspicious in ways not consistent with what they did after past
outbreaks.

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

--
Bill Sloman, Sydney

 

On Thursday, April 30, 2020 at 9:54:04 PM UTC-4, Bill Sloman wrote:

On Friday, May 1, 2020 at 3:13:09 AM UTC+10, bloggs.fre...@gmail.com wrote:
On Thursday, April 30, 2020 at 10:59:13 AM UTC-4, Bill Sloman wrote:
On Friday, May 1, 2020 at 12:03:47 AM UTC+10, bloggs.fre...@gmail.com wrote:
On Thursday, April 30, 2020 at 9:25:12 AM UTC-4, Bill Sloman wrote:
On Thursday, April 30, 2020 at 9:04:42 PM UTC+10, bloggs.fre...@gmail.com wrote:
On Wednesday, April 29, 2020 at 9:00:03 PM UTC-4, Bill Sloman wrote:
On Thursday, April 30, 2020 at 10:24:35 AM UTC+10, bloggs.fre....@gmail.com wrote:
On Wednesday, April 29, 2020 at 7:22:13 PM UTC-4, Bill Sloman wrote:
On Thursday, April 30, 2020 at 1:50:47 AM UTC+10, bloggs.fre...@gmail.com wrote:
On Wednesday, April 29, 2020 at 11:27:11 AM UTC-4, jla....@highlandsniptechnology.com wrote:
On Wed, 29 Apr 2020 07:49:09 -0700 (PDT),
bloggs.fredbloggs.fred@gmail.com wrote:

On Wednesday, April 29, 2020 at 10:38:21 AM UTC-4, jla...@highlandsniptechnology.com wrote:
On Wed, 29 Apr 2020 05:25:30 -0700 (PDT),
bloggs.fredbloggs.fred@gmail.com wrote:

snip

C19 could be natural. All the previous centuries of colds and flu
were. We get colds and flu every winter.

Not likely to be natural, it's too optimized for human infection.

Natural selection is perfectly natural, and any virus that 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, it's going to look optimised for the job.

What's special about Covid-19 that has suggested - to anybody who knows what they are talking about - that it's had the benefit of intelligent design by humans?

Fred Bloggs clearly doesn't know what he is talking about, so hi opinion doesn't count.

So says Sloman who has been wrong about every last aspect of this whole fiasco since day one. His ignorance and errors are too numerous to list.

Whereas I have cited a few points where Fred Bloggs has made claims that illustrate that he doesn't know what he is talking about.

He claimed that the corona virus spike protein doesn't mutate - 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 follow 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.

snipped Fred being even more stupid than usual

Once again you couldn't be more wrong. No one cares about any general description 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 addresses that bizarre oversight.

The people who actually work with this virus, with the aim of actually accomplishing something, have narrowed their focus on the ACE-2 receptor binding domain (RBD) of the spike protein.

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

They find the RBD to be "highly conserved," so much so that they were able 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 talking about. The vaccine that was being developed against SARS is also active against Covid-19, although the antigen being synthesised should be tweaked to make the antibody evoked one that was slightly more active against Covid-19.

https://www.pnas.org/content/pnas/117/15/8218.full.pdf

See antibody CR3022 as one example of an antibody targeting the spike protein of both SARS-CoV-1 and SARS-CoV-2, despite a genetic overlap of just 79% between the two viruses.

The overlap is over the whole 33k length of genome. The interesting question 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 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.

The CR3022 antibody is referred to in a 2006 paper

https://www.ncbi.nlm.nih.gov/pubmed/16796401

It was harvested from a patient who had recovered from SARS so it doesn't 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 does depend on what the antibody is looking for.

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

Perhaps.

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 technology.

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

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


https://www.pnas.org/content/pnas/117/15/8218.full.pdf

"“That really killed RSV vaccines for a generation,”says Peter 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 globally nearly two decades ago, Hotez was among researchers who began investigating a potential vaccine. In early tests of his candidate, he witnessed 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 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 protein 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 paper 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 genetic 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.

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

https://en.wikipedia.org/wiki/Angiotensin-converting_enzyme_2

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

the antibody is going to lock onto the same protein. This doesn't follow. 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 the receptor binding domain in a way that made the antibody that recogised it less 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 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 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 vectors before they have a chance to infect cells, or killing infecting cells before they have a chance to produce antigen?

--
Bill Sloman, Sydney

 

[John Larkin]

On Fri, 1 May 2020 07:16:31 -0700 (PDT), Whoey Louie
<trader4@optonline.net> wrote:

On Wednesday, April 29, 2020 at 7:22:13 PM UTC-4, Bill Sloman wrote:
On Thursday, April 30, 2020 at 1:50:47 AM UTC+10, bloggs.fre...@gmail.com wrote:
On Wednesday, April 29, 2020 at 11:27:11 AM UTC-4, jla...@highlandsniptechnology.com wrote:
On Wed, 29 Apr 2020 07:49:09 -0700 (PDT),
bloggs.fredbloggs.fred@gmail.com wrote:

On Wednesday, April 29, 2020 at 10:38:21 AM UTC-4, jla...@highlandsniptechnology.com wrote:
On Wed, 29 Apr 2020 05:25:30 -0700 (PDT),
bloggs.fredbloggs.fred@gmail.com wrote:

snip

C19 could be natural. All the previous centuries of colds and flu
were. We get colds and flu every winter.

Not likely to be natural, it's too optimized for human infection.

Natural selection is perfectly natural, and any virus that 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, it's going to look optimised for the job.

What's special about Covid-19 that has suggested - to anybody who knows what they are talking about - that it's had the benefit of intelligent design by humans?

Fred Bloggs clearly doesn't know what he is talking about, so hi opinion doesn't count.

--
Bill Sloman, Sydney

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.

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.


--

John Larkin Highland Technology, Inc
picosecond timing precision measurement

jlarkin att highlandtechnology dott com
http://www.highlandtechnology.com

 

Ricky C <gnuarm.deletethisbit@gmail.com> wrote in
news:356ac91b-6e82-4c45-a306-8bffb9c8d871@googlegroups.com:

On Friday, May 1, 2020 at 10:08:35 AM UTC-4, HooHeeTardHee wrote:

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.

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

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)

 

On Friday, May 1, 2020 at 12:23:09 PM UTC-4, John Larkin wrote:

On Fri, 1 May 2020 07:16:31 -0700 (PDT), Whoey Louie
trader4@optonline.net> wrote:

On Wednesday, April 29, 2020 at 7:22:13 PM UTC-4, Bill Sloman wrote:
On Thursday, April 30, 2020 at 1:50:47 AM UTC+10, bloggs.fre...@gmail.com wrote:
On Wednesday, April 29, 2020 at 11:27:11 AM UTC-4, jla...@highlandsniptechnology.com wrote:
On Wed, 29 Apr 2020 07:49:09 -0700 (PDT),
bloggs.fredbloggs.fred@gmail.com wrote:

On Wednesday, April 29, 2020 at 10:38:21 AM UTC-4, jla...@highlandsniptechnology.com wrote:
On Wed, 29 Apr 2020 05:25:30 -0700 (PDT),
bloggs.fredbloggs.fred@gmail.com wrote:

snip

C19 could be natural. All the previous centuries of colds and flu
were. We get colds and flu every winter.

Not likely to be natural, it's too optimized for human infection.

Natural selection is perfectly natural, and any virus that 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, it's going to look optimised for the job.

What's special about Covid-19 that has suggested - to anybody who knows what they are talking about - that it's had the benefit of intelligent design by humans?

Fred Bloggs clearly doesn't know what he is talking about, so hi opinion doesn't count.

--
Bill Sloman, Sydney

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.


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.

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.

https://news.emory.edu/stories/2020/04/covid_eidd2801_fda/index.html

--

John Larkin Highland Technology, Inc
picosecond timing precision measurement

jlarkin att highlandtechnology dott com
http://www.highlandtechnology.com