OT: Gov wants to kill us..

On Tue, 05 Aug 2014 18:18:27 -0700, John Larkin
<jjlarkin@highNOTlandTHIStechnologyPART.com> wrote:

On Tue, 05 Aug 2014 18:36:27 -0400, krw@attt.bizz wrote:

On Mon, 04 Aug 2014 19:23:55 -0700, John Larkin
jjlarkin@highNOTlandTHIStechnologyPART.com> wrote:

On Mon, 04 Aug 2014 19:31:23 -0400, krw@attt.bizz wrote:

On Mon, 04 Aug 2014 16:09:31 -0700, John Larkin
jlarkin@highlandtechnology.com> wrote:

On Mon, 04 Aug 2014 18:45:36 -0400, krw@attt.bizz wrote:

On Mon, 04 Aug 2014 11:41:16 -0700, John Larkin
jlarkin@highlandtechnology.com> wrote:

On Mon, 04 Aug 2014 14:10:57 -0400, krw@attt.bizz wrote:

On Mon, 4 Aug 2014 06:45:11 -0700 (PDT), dagmargoodboat@yahoo.com
wrote:

On Monday, August 4, 2014 8:56:54 AM UTC-4, David Brown wrote:
On 03/08/14 19:23, fredbloggs wrote:
On Sunday, August 3, 2014 1:13:21 PM UTC-4, John Larkin wrote:


Maybe they can save their lives.

They have saved their lives, we have expensive therapies not
available in Africa. They're both improving and will be fully
recovered soon.

The treatment in the USA is the same as the treatment in African
hospitals - intravenous fluids and try to make the patient comfortable.
Like many virus infections, there are no medical treatments involved -
you just treat the symptoms and help the patient's own immune system do
its job. So the survival rates for ebola patients in the USA are not
much higher than for African hospitals

We've never had a case in the USA.

(though of course they are less
likely to suffer secondary problems, such as getting something else due
to lack of sterilised equipment).

There are experimental treatments for ebola, such as blood transfusions
from ebola survivors (hopefully with some useful antibodies), but I
don't think they are being used in these cases.

Dr. Brantly got such a transfusion, in gratitude, from one of the patients he saved.

No, it was the woman who got the experimental treatment. Dr. Brantly
was offered the treatment but said that she was in worse shape so
needed it more.

Further developments:

http://www.cnn.com/2014/08/04/health/experimental-ebola-serum/index.html

Yes, I saw that after I had posted. Seems they're not telling
everyone what's happening, even here. People are pissed.

Not me!

You aren't all people and you don't live in Atlanta.

There are several labs in the US that are working on ebola. The serem that they
gave to those two doctors was made by a company in San Diego. Ebola is here.

Contagious people were *NOT* here before Sunday. That's the point. I
would trust a private company before the CDC. The CDC has proven
themselves to be incompetent. No surprise - government employees.

There will be real, non-isolated, wandering-around ebola carriers here sooner or
later, probably sooner. And the chances of you getting infected are minute. So
relax.

Of course you miss the point entirely.
 
On 06/08/14 00:38, krw@attt.bizz wrote:
On Mon, 4 Aug 2014 19:35:40 -0700 (PDT), dagmargoodboat@yahoo.com
wrote:

On Monday, August 4, 2014 6:50:29 PM UTC-4, k...@attt.bizz wrote:
On Mon, 4 Aug 2014 14:09:25 -0700 (PDT), dagmargoo...@yahoo.com wrote:
On Monday, August 4, 2014 4:56:47 PM UTC-4, bloggs.fred...@gmail.com wrote:
On Monday, August 4, 2014 4:45:31 PM UTC-4, dagmarg...@yahoo.com wrote:

http://abcnews.go.com/Health/WorldNews/ebola-stricken-american-doctor-turn-worse/story?id=24791024

That story is old and inaccurate. Originally he wanted the female to get the serum because he seemed better off. Then his condition rapidly deteriorated and they gave him the serum first.

Yep. Thanks for the correction.

The news was just reporting that both had received two doses of the
serum. The first didn't do much but the second made a big difference
in both. Dr. Brandtly reportedly walked (with help) from the
ambulance into the hospital and she was now well enough to fly (should
be here tomorrow).

I'm not worried about transmission--you've pretty well got to touch someone
to get it--but for people who worry...the serum came from San Diego.

The two doctors worked in full hazmat gear. How did they get it?
There is a lot that's not being said, here.

Haven't you seen "Outbreak"? Even with full hazmat gear, accidents can
happen.

Actually, the ebola health care workers in Africa do not wear "full
hazmat gear" (as used in biolabs) - it would be impossible to work in in
that environment. They mostly wear masks, glasses, coveralls, gloves
and boots. The chances of ebola virus particles getting in somewhere
along the line (including the process of taking the cloths off at the
end of the shift) are small, but not negligible.

So basically they were unlucky - there is no need (at this stage) to
worry that there is some unknown transmission vector.


So, they've got virus too. Maybe that Spanish flu professor in
Minnesota can get in the game and make a super-er influbola bug.

Sounds about par.
 
On 06/08/14 03:33, rickman wrote:
On 8/5/2014 9:18 PM, John Larkin wrote:

There will be real, non-isolated, wandering-around ebola carriers here
sooner or
later, probably sooner. And the chances of you getting infected are
minute. So
relax.

I'm not trying to make any comparisons and I'm not trying to raise any
alarms, but similar things have happened with other, much more common
diseases. There were cases of malaria reported in people from the area
around Dullas airport near DC who had never been outside the country.
I'm not sure if it was a guess or what, but they figured someone who had
just come from Africa was bitten by mosquito(s) which in turn infected
locals. Those are the only cases of home grown malaria I have ever
heard of and malaria is a *very* common disease in Africa.

There are regularly small local outbreaks like this in the USA, because
there are mosquitoes in the USA that are able to transmit malaria.
Since endemic malaria was eliminated in the USA the source of such local
outbreaks is always going to be an person who was infected outside the
country.


Ebola is a very different sort of disease, with very different ways of
spreading. I don't expect it to have a serious direct effect in any
western country - but I /do/ expect there will be indirect effects -
i.e., fear and panic from it.
 
On Wednesday, 6 August 2014 14:46:45 UTC+10, dagmarg...@yahoo.com wrote:
On Tuesday, August 5, 2014 5:03:38 PM UTC-4, bloggs.fred...@gmail.com wrote:
On Tuesday, August 5, 2014 4:35:13 PM UTC-4, dagmarg...@yahoo.com wrote:

You're arguing that hyper-accelerated artificially-directed human-targeted viral evolution is no worse than what would've happened naturally.

That's idiotic.

There's no such thing as "hyper-accelerated artificially-directed human-targeted viral evolution"- you're reading too much science fiction.

They're selectively breeding virii for virulence, and specifically to
evade human immune systems.

The only selection going on is that if a virus doesn't infect the test animal - a ferret, not a human - it doesn't get propagated. There's no human immune system involved, though they wouldn't be using ferrets if the ferret immune system was wildly different from the human immune system.

The selection going on is pretty much what happens in the wild - although the flu virus is a bird virus that can jump to pigs and humans, so it does live in a different environment. The virus has only one interest - to have as many offspring as possible. We get interested when the side effects of the infection kill a significant proportion of the humans infected. This is actually bad from the point of view of the virus, because it wants it's host to be active and spreading new virii for as long as possible

> How on earth is that not an orders-of-magnitude faster selection mechanism compared to random chance?

Where's the difference between what's going on lab and what's going on in the wild? The mutations are being produced by the same random mechanism, and the only difference is in the selection of hosts on offer.

Admittedly, the actual mutations happen in the host cell, after it has been infected by the virus, while the genetic information introduced by the virus is being turned into a new generation of virii the cell's hijacked replication machinery, so the choice of host cell may make some difference.

Sadly for your credibility there are no "orders of magnitude" differences on offer - that all comes from your over-active and under-informed imagination.

> James (Chicken Little) Arthur

--
Bill Sloman, Sydney
 
On 8/6/2014 2:16 AM, David Brown wrote:
On 06/08/14 03:33, rickman wrote:

I'm not trying to make any comparisons and I'm not trying to raise any
alarms, but similar things have happened with other, much more common
diseases. There were cases of malaria reported in people from the area
around Dullas airport near DC who had never been outside the country.
I'm not sure if it was a guess or what, but they figured someone who had
just come from Africa was bitten by mosquito(s) which in turn infected
locals. Those are the only cases of home grown malaria I have ever
heard of and malaria is a *very* common disease in Africa.


There are regularly small local outbreaks like this in the USA, because
there are mosquitoes in the USA that are able to transmit malaria.
Since endemic malaria was eliminated in the USA the source of such local
outbreaks is always going to be an person who was infected outside the
country.


Ebola is a very different sort of disease, with very different ways of
spreading. I don't expect it to have a serious direct effect in any
western country - but I /do/ expect there will be indirect effects -
i.e., fear and panic from it.

Yes, what most people don't understand is that mosquitoes are not little
hypodermic needles. For them to infect a person the parasite has to
infect the mosquito as part of it's life cycle. So Ebola can't be
spread by mosquitoes.

--

Rick
 
On Wednesday, August 6, 2014 5:20:13 AM UTC-4, Bill Sloman wrote:
On Wednesday, 6 August 2014 14:46:45 UTC+10, dagmarg...@yahoo.com wrote:
On Tuesday, August 5, 2014 5:03:38 PM UTC-4, bloggs.fred...@gmail.com wrote:
On Tuesday, August 5, 2014 4:35:13 PM UTC-4, dagmarg...@yahoo.com wrote:

You're arguing that hyper-accelerated artificially-directed human-targeted viral evolution is no worse than what would've happened naturally.

That's idiotic.

There's no such thing as "hyper-accelerated artificially-directed human-targeted viral evolution"- you're reading too much science fiction.

They're selectively breeding virii for virulence, and specifically to
evade human immune systems.

The only selection going on is that if a virus doesn't infect the test animal - a ferret, not a human - it doesn't get propagated. There's no human immune system involved, though they wouldn't be using ferrets if the ferret immune system was wildly different from the human immune system.

The effort was to create a more TRANSMISSIBLE virus, more LETHAL, and
one that evades HUMAN immunity.

-----
http://www.independent.co.uk/news/science/exclusive-controversial-us-scientist-creates-deadly-new-flu-strain-for-pandemic-research-9577088.html

Some members of the audience, however, were shocked and astonished at his latest and most audacious work on flu viruses, which follow on from his attempts to re-create the 1918 flu virus and an earlier project to increase the TRANSMISSIBILITY of a highly lethal strain of bird flu.

"He took the 2009 pandemic flu virus and selected out strains that were not neutralised by HUMAN antibodies. He repeated this several times until he got a real humdinger of a virus," said one scientist who was present at Professor Kawaoka's talk.

"He left no doubt in my mind that he had achieved it. He used a flu virus that is known to infect HUMANS and then manipulated it in such a way that it would effectively leave the global population defenceless if it ever escaped from his laboratory," he said.

"He's basically got a known pandemic strain that is now resistant to vaccination. Everything he did before was dangerous but this is even madder. This is the virus," he added.
----


The selection going on is pretty much what happens in the wild - although the flu virus is a bird virus that can jump to pigs and humans, so it does live in a different environment. The virus has only one interest - to have as many offspring as possible. We get interested when the side effects of the infection kill a significant proportion of the humans infected. This is actually bad from the point of view of the virus, because it wants it's host to be active and spreading new virii for as long as possible

How on earth is that not an orders-of-magnitude faster selection mechanism compared to random chance?

Where's the difference between what's going on lab and what's going on in the wild? The mutations are being produced by the same random mechanism, and the only difference is in the selection of hosts on offer.

Admittedly, the actual mutations happen in the host cell, after it has been infected by the virus, while the genetic information introduced by the virus is being turned into a new generation of virii the cell's hijacked replication machinery, so the choice of host cell may make some difference.

Sadly for your credibility there are no "orders of magnitude" differences on offer - that all comes from your over-active and under-informed imagination.

James (Chicken Little) Arthur

You're contradicting yourself.

If there's no difference in rate, there'd no need for the artificial
selection to start with--it would already exist.

If there's no difference in selection pressure, why hasn't the new
strain emerged despite a century in the wild?

If there's no difference in rate, how was Kawaoka able to create exactly
what he wanted in just a few years, something nature hasn't yielded in a
century?

Isn't that orders-of-magnitude right there? Of course it is. Q.E.D.

You correctly said earlier that the *natural* selection pressure is for less
virulence over time, yet insist here a retrograde selection is no different
from the natural selection pressure. It isn't.

-----
http://www.cdc.gov/flu/about/qa/1918flupandemic.htm
"It is impossible to predict with certainly, but the probability of the 1918 virus re-emerging from a natural source appears to be remote."

[...]

"Are current antivirals and vaccines effective against the 1918 virus?

Yes. Two types of antiviral drugs, rimantadine (Flumadine) and oseltamivir (Tamiflu), have been shown to be effective "
----

So, the CDC opines the Franken-strain was unlikely to emerge, and if it
did we've got herd immunity and drugs that help.

Kawaoka's work was to defeat and reverse those natural outcomes. That
is, by definition, unnatural.

You remind me of a friend's wife who had something to prove, and challenged
me to a word game she enjoyed. She lost. Hundreds and hundreds of times,
game after game, set after set, over years. She never won, not even once,
not a single game. With practice (playing her), the outcomes just got more
lop-sided.

She, positive it was luck, was dead-set on proving it. And the more she
lost, the more certain she became, and the more determined to prove it.


Cheers,
James Arthur
 
On Wednesday, August 6, 2014 12:52:08 AM UTC-4, dagmarg...@yahoo.com wrote:
On Tuesday, August 5, 2014 11:20:58 PM UTC-4, bloggs.fred...@gmail.com wrote:

On Tuesday, August 5, 2014 8:57:41 PM UTC-4, Phil Hobbs wrote:



Doubtless, but that has nothing to do with what I was talking about,

namely the question of whether the CDC folks can find their collective

derrieres with two hands, a map, DNA sequencers, radar, etc.



Is this opinion coming from your reading of that sensationalistic Hotpants book?



"The Hot Zone" was published seven years before the anthrax attacks.

Looks like his The Demon in the Freezer pretends to an historical account. Looking at his Amazon page the Preston character is just another fear monger. He really has his nerve saying this pulp trash of his are "true" stories, and look at the publishers. I don't see that he has the educational background or professional experience to be taken seriously. Anyone can see from the ebook previews that his work is on the level of comic books.

You don't know anything about the CDC and all the stuff they're tasked with GLOBALLY.

The real idiot here is whoever tasked the CDC to determine if the sample was "weaponized"- not really central to their expertise in disease control.



Cheers,

James Arthur
 
On Wednesday, August 6, 2014 12:52:08 AM UTC-4, dagmarg...@yahoo.com wrote:
On Tuesday, August 5, 2014 11:20:58 PM UTC-4, bloggs.fred...@gmail.com wrote:

On Tuesday, August 5, 2014 8:57:41 PM UTC-4, Phil Hobbs wrote:



Doubtless, but that has nothing to do with what I was talking about,

namely the question of whether the CDC folks can find their collective

derrieres with two hands, a map, DNA sequencers, radar, etc.



Is this opinion coming from your reading of that sensationalistic Hotpants book?



"The Hot Zone" was published seven years before the anthrax attacks.



You don't know anything about the CDC and all the stuff they're tasked with GLOBALLY.

The real idiot here is whoever tasked the CDC to determine if the sample was "weaponized"- not really central to their expertise in disease control.



Cheers,

James Arthur

This book is for anyone who thinks the DoD is anything another than a major fraud. It is very well researched and, above all, factual:

Vaccine A: The Covert Government Experiment That's Killing Our Soldiers--and Why GI's Are Only the First Victims... by Gary Matsumoto (Aug 10, 2010)

Note that the circulation is vastly reduced because it debunks what people want to believe. Bottom line is you don't want the military anywhere near public health.
 
On Wednesday, 6 August 2014 22:56:46 UTC+10, dagmarg...@yahoo.com wrote:
On Wednesday, August 6, 2014 5:20:13 AM UTC-4, Bill Sloman wrote:
On Wednesday, 6 August 2014 14:46:45 UTC+10, dagmarg...@yahoo.com wrote:
On Tuesday, August 5, 2014 5:03:38 PM UTC-4, bloggs.fred...@gmail.com wrote:
On Tuesday, August 5, 2014 4:35:13 PM UTC-4, dagmarg...@yahoo.com wrote:

You're arguing that hyper-accelerated artificially-directed human-targeted viral evolution is no worse than what would've happened naturally..

That's idiotic.

There's no such thing as "hyper-accelerated artificially-directed human-targeted viral evolution"- you're reading too much science fiction.

They're selectively breeding virii for virulence, and specifically to
evade human immune systems.

The only selection going on is that if a virus doesn't infect the test animal - a ferret, not a human - it doesn't get propagated. There's no human immune system involved, though they wouldn't be using ferrets if the ferret immune system was wildly different from the human immune system.

The effort was to create a more TRANSMISSIBLE virus, more LETHAL, and one that evades HUMAN immunity.

No. The effort was to see what natural variation could produce in the way of a more transmissible virus. The scientist involved kept track of the mutations that appeared in his laboratory population. There's no suggestion that even he did anything to get more mutations - there's no need since if virii mutated any faster, they'd die out.
http://www.independent.co.uk/news/science/exclusive-controversial-us-scientist-creates-deadly-new-flu-strain-for-pandemic-research-9577088.html

UK science journalists don't know what they are talking about, any more than you do. The scientist involved didn't "create" anything - he just documented what he found in the virus population that existed in his lab. The wild type virus will eventually get around to producing a variant with much the same collection of properties.

The difference is that we'll find out about that when it starts killing people, rather than ferrets.

> Some members of the audience, however, were shocked and astonished at his latest and most audacious work on flu viruses, which follow on from his attempts to re-create the 1918 flu virus and an earlier project to increase the TRANSMISSIBILITY of a highly lethal strain of bird flu.

Not exactly increasing the transmissiblity, but rather monitoring his laboratory population to see what it would throw up in the way of more transmissible virii.

You've got this ill-informed idea that we know the fine details of how the virus works in the cell and could manipulate the genetic information to make it work better. Neither happens to be true, so you are having hysterics about a boogey-man that only exists in your imagination.

> "He took the 2009 pandemic flu virus and selected out strains that were not neutralised by HUMAN antibodies. He repeated this several times until he got a real humdinger of a virus," said one scientist who was present at Professor Kawaoka's talk.

That how the reporter understood what was said. The reporter seems to be as il-informed as you are.

> "He left no doubt in my mind that he had achieved it. He used a flu virus that is known to infect HUMANS and then manipulated it in such a way that it would effectively leave the global population defenceless if it ever escaped from his laboratory," he said.

Kawaoka didn't "manipulate" anything. He found a virus that was better at infecting ferrets than anything else that he could get his hands on.

> "He's basically got a known pandemic strain that is now resistant to vaccination. Everything he did before was dangerous but this is even madder. This is the virus," he added.

Every year the wild type virus has mutated enough that last year's vaccines don't work. It seems unlikely that the reporter correctly understood what was being said.

The selection going on is pretty much what happens in the wild - although the flu virus is a bird virus that can jump to pigs and humans, so it does live in a different environment. The virus has only one interest - to have as many offspring as possible. We get interested when the side effects of the infection kill a significant proportion of the humans infected. This is actually bad from the point of view of the virus, because it wants it's host to be active and spreading new virii for as long as possible

How on earth is that not an orders-of-magnitude faster selection mechanism compared to random chance?

Where's the difference between what's going on lab and what's going on in the wild? The mutations are being produced by the same random mechanism, and the only difference is in the selection of hosts on offer.

Admittedly, the actual mutations happen in the host cell, after it has been infected by the virus, while the genetic information introduced by the virus is being turned into a new generation of virii the cell's hijacked replication machinery, so the choice of host cell may make some difference.

Sadly for your credibility there are no "orders of magnitude" differences on offer - that all comes from your over-active and under-informed imagination.

James (Chicken Little) Arthur

You're contradicting yourself.

If there's no difference in rate, there'd no need for the artificial selection to start with--it would already exist.

Not exactly. There's basic selection - in that most mutations are lethal - and the researcher gets to look at his surviving population and can pick out strains that seem to propagate faster or make the ferrets sneeze more frequently, and selectively propagate them. He can pick which populations he continues to watch for new variations, but he can't really chance the rate of variation. If he did increase there'd be too many lethal mutations and the strain would die out.

> If there's no difference in selection pressure, why hasn't the new strain emerged despite a century in the wild?

There are new strains all the time. Spanish flu was both lethal and transmissible. H7N9 chicken flu is lethal, but not transmissible between humans.

If you have a lab population that started out with H7N9 you can look at what it does when it throws up more ferret-transmissible variants, and sequence them. It's all information. If we do enough of it we may get to understand why some variants are more transmissible or more lethal
If there's no difference in rate, how was Kawaoka able to create exactly
what he wanted in just a few years, something nature hasn't yielded in a
century?

He didn't "create exactly what he wanted". He found some variants that he could describe in a way that frightened the life out of unsophisticated science journalists and won him a lot of column inches.

> Isn't that orders-of-magnitude right there? Of course it is. Q.E.D.

This is the same gullible James Arthur who believes everything the denialist propaganda mill churns out. He hasn't notice that good news doesn't sell newspapers, and "end of the world stories" do, no matter how implausible they are.

You correctly said earlier that the *natural* selection pressure is for less virulence over time, yet insist here a retrograde selection is no different
from the natural selection pressure. It isn't.

Selection pressure is just picking winners. More pressure doesn't produce more variation, or a different range of variations.

http://www.cdc.gov/flu/about/qa/1918flupandemic.htm

"It is impossible to predict with certainly, but the probability of the 1918 virus re-emerging from a natural source appears to be remote."

Of course it is. The next version of flu that is as lethal and transmissible as the 1918 Spanish flu will probably have found different ways to be particularly transmissible and particularly lethal.

"Are current antivirals and vaccines effective against the 1918 virus?

Yes. Two types of antiviral drugs, rimantadine (Flumadine) and oseltamivir (Tamiflu), have been shown to be effective "


So, the CDC opines the Franken-strain was unlikely to emerge, and if it did we've got herd immunity and drugs that help.

The 1918 flu stopped being a problem after 1918 because enough people had herd immunity - in fact it's hypothesised that it mainly killed young people because older people had already been exposed to a closely related strain, and their immune systems recognised and dealt with the Spanish flu virus before it could infect them.

> Kawaoka's work was to defeat and reverse those natural outcomes. That is, by definition, unnatural.

No. There's nothing natural about Tamiflu, and it doesn't look as if we've had any flu strains that were close to the 1918 strain for several generations now.

My mother was born in 1918, and could have been exposed, but she die last year at 95.

Kawaoka's work was aimed at seeing how the current strains could get to be more transmissible or more lethal. It was essentially observational. There's nothing unnatural about looking at the way a captive population evolves.

> You remind me of a friend's wife who had something to prove, and challenged me to a word game she enjoyed. She lost. Hundreds and hundreds of times,
game after game, set after set, over years. She never won, not even once, not a single game. With practice (playing her), the outcomes just got more
lop-sided.
She, positive it was luck, was dead-set on proving it. And the more she lost, the more certain she became, and the more determined to prove it.

It is much the same situation, but here it is you who is losing - because you don't know what you are talking about.

You are convinced that by citing alarmist journalists who don't what they are talking about either you can persuade the rest of world that you've got the right end of the stick, but all your determination is doing for you is building up a thicker layer of egg all over your face.

The UK Independent is a "quality newspaper" in the sense that it takes itself seriously and doesn't publish pictures of under-dressed young women, but it isn't actually all that good. If you want English language science reporting, read New Scientist - it's more or less reliable. We've had a subscription for about thirty years now, and it doesn't get stuff wrong all that often.

You wouldn't like it - it accepts the scientific case for anthropogenic global warming, and has been known to take climate modelling almost seriously.

--
Bill Sloman, Sydney
 
On Thursday, 7 August 2014 01:13:39 UTC+10, Jeroen Belleman wrote:
On 2014-08-06 11:20, Bill Sloman wrote:
On Wednesday, 6 August 2014 14:46:45 UTC+10, dagmarg...@yahoo.com
wrote:
On Tuesday, August 5, 2014 5:03:38 PM UTC-4,
bloggs.fred...@gmail.com wrote:
On Tuesday, August 5, 2014 4:35:13 PM UTC-4, dagmarg...@yahoo.com
wrote:

You're arguing that hyper-accelerated artificially-directed
human-targeted viral evolution is no worse than what would've
happened naturally.

That's idiotic.

There's no such thing as "hyper-accelerated artificially-directed
human-targeted viral evolution"- you're reading too much science
fiction.

They're selectively breeding virii for virulence, and specifically
to evade human immune systems.

How on earth is that not an orders-of-magnitude faster selection mechanism compared to random chance?

Where's the difference between what's going on lab and what's going on in the wild? The mutations are being produced by the same random mechanism, and the only difference is in the selection of hosts on offer.

Admittedly, the actual mutations happen in the host cell, after it has been infected by the virus, while the genetic information introduced by the virus is being turned into a new generation of virii the cell's hijacked replication machinery, so the choice of host cell may make some difference..

Sadly for your credibility there are no "orders of magnitude" differences on offer - that all comes from your over-active and under-informed imagination.

James (Chicken Little) Arthur

You can considerably speed up virus mutations by infecting cells with multiple viruses. The new generation of virii easily incorporates bits of foreign NA, possibly picking up new talents in doing so. While in nature this happens only by chance, in the lab this can be arranged on purpose, and
with specific targets in mind. That's a far cry from random mutation.

Perhaps. Multiple viruses hitting the cell all at once are all going to be trying to take over the cells replicating machinery at the same time. The likeliest outcome is a very dead cell and no new viruses. You may be lucky and get a surviving hybrid, but you'd have to be very lucky to get one that could take over another cell and produce copies of itself.

Producing one that was as viable as the flu virus would be an even longer stretch.

--
Bill Sloman, Sydney
 
On Wednesday, August 6, 2014 11:13:39 AM UTC-4, Jeroen Belleman wrote:
On 2014-08-06 11:20, Bill Sloman wrote:

On Wednesday, 6 August 2014 14:46:45 UTC+10, dagmarg...@yahoo.com

wrote:

On Tuesday, August 5, 2014 5:03:38 PM UTC-4,

bloggs.fred...@gmail.com wrote:

On Tuesday, August 5, 2014 4:35:13 PM UTC-4, dagmarg...@yahoo.com

wrote:



You're arguing that hyper-accelerated artificially-directed

human-targeted viral evolution is no worse than what would've

happened naturally.



That's idiotic.



There's no such thing as "hyper-accelerated artificially-directed

human-targeted viral evolution"- you're reading too much science

fiction.



They're selectively breeding virii for virulence, and specifically

to

evade human immune systems.



How on earth is that not an orders-of-magnitude faster selection

mechanism compared to random chance?



Where's the difference between what's going on lab and what's going

on in the wild? The mutations are being produced by the same random

mechanism, and the only difference is in the selection of hosts on

offer.



Admittedly, the actual mutations happen in the host cell, after it

has been infected by the virus, while the genetic information

introduced by the virus is being turned into a new generation of

virii the cell's hijacked replication machinery, so the choice of

host cell may make some difference.



Sadly for your credibility there are no "orders of magnitude"

differences on offer - that all comes from your over-active and

under-informed imagination.



James (Chicken Little) Arthur





You can considerably speed up virus mutations by infecting

cells with multiple viruses. The new generation of virii

easily incorporates bits of foreign NA, possibly picking up

new talents in doing so. While in nature this happens only

by chance, in the lab this can be arranged on purpose, and

with specific targets in mind. That's a far cry from random

mutation.

Insofar as our understanding of the effects of the new genetic material, it is a random mutation. This is done all the time with the so-called DNA vaccine developments, incorporating a gene or two from a very lethal virus into the nucleus of a less lethal virus in the hopes the lethal virus gene protein expression will train the immune response to recognize and effectively attack the same protein when presented with an infection with the lethal virus. This technique is only rarely successful. Time to get back to tidying up the lab for your masters now...go on, little boy.

Jeroen Belleman
 
On Wednesday, August 6, 2014 1:30:41 PM UTC-4, k...@attt.bizz wrote:

All of them? GMAFB!

It's always you worthless people who are so in fear of their life...
 
On Wednesday, August 6, 2014 12:30:46 PM UTC-4, Bill Sloman wrote:
On Thursday, 7 August 2014 01:13:39 UTC+10, Jeroen Belleman wrote:

On 2014-08-06 11:20, Bill Sloman wrote:

On Wednesday, 6 August 2014 14:46:45 UTC+10, dagmarg...@yahoo.com

wrote:

On Tuesday, August 5, 2014 5:03:38 PM UTC-4,

bloggs.fred...@gmail.com wrote:

On Tuesday, August 5, 2014 4:35:13 PM UTC-4, dagmarg...@yahoo.com

wrote:



You're arguing that hyper-accelerated artificially-directed

human-targeted viral evolution is no worse than what would've

happened naturally.



That's idiotic.



There's no such thing as "hyper-accelerated artificially-directed

human-targeted viral evolution"- you're reading too much science

fiction.



They're selectively breeding virii for virulence, and specifically

to evade human immune systems.



How on earth is that not an orders-of-magnitude faster selection mechanism compared to random chance?



Where's the difference between what's going on lab and what's going on in the wild? The mutations are being produced by the same random mechanism, and the only difference is in the selection of hosts on offer.



Admittedly, the actual mutations happen in the host cell, after it has been infected by the virus, while the genetic information introduced by the virus is being turned into a new generation of virii the cell's hijacked replication machinery, so the choice of host cell may make some difference.



Sadly for your credibility there are no "orders of magnitude" differences on offer - that all comes from your over-active and under-informed imagination.



James (Chicken Little) Arthur



You can considerably speed up virus mutations by infecting cells with multiple viruses. The new generation of virii easily incorporates bits of foreign NA, possibly picking up new talents in doing so. While in nature this happens only by chance, in the lab this can be arranged on purpose, and

with specific targets in mind. That's a far cry from random mutation.



Perhaps. Multiple viruses hitting the cell all at once are all going to be trying to take over the cells replicating machinery at the same time. The likeliest outcome is a very dead cell and no new viruses. You may be lucky and get a surviving hybrid, but you'd have to be very lucky to get one that could take over another cell and produce copies of itself.



Producing one that was as viable as the flu virus would be an even longer stretch.

These complex hybrid virus things, also known as chimeric virus, are usually very short lived, meaning they have an hour or so to find a host cell and reproduce before they become just a dead particle. The wild strains naturally occurring in nature represent optimum biochemical entities, any perturbation results in a crippled entity of some sort. There has been serious research for at least 20 years that I know of, into deliberately introducing therapy that enhances the randomization of the viral structures so that the freak variants will crowd out the wild strain, suppressing if not entirely eliminating its reproductive opportunities, after which the freaks are allowed to die out naturally.

--

Bill Sloman, Sydney
 
On 2014-08-06 11:20, Bill Sloman wrote:
On Wednesday, 6 August 2014 14:46:45 UTC+10, dagmarg...@yahoo.com
wrote:
On Tuesday, August 5, 2014 5:03:38 PM UTC-4,
bloggs.fred...@gmail.com wrote:
On Tuesday, August 5, 2014 4:35:13 PM UTC-4, dagmarg...@yahoo.com
wrote:

You're arguing that hyper-accelerated artificially-directed
human-targeted viral evolution is no worse than what would've
happened naturally.

That's idiotic.

There's no such thing as "hyper-accelerated artificially-directed
human-targeted viral evolution"- you're reading too much science
fiction.

They're selectively breeding virii for virulence, and specifically
to
evade human immune systems.

How on earth is that not an orders-of-magnitude faster selection
mechanism compared to random chance?

Where's the difference between what's going on lab and what's going
on in the wild? The mutations are being produced by the same random
mechanism, and the only difference is in the selection of hosts on
offer.

Admittedly, the actual mutations happen in the host cell, after it
has been infected by the virus, while the genetic information
introduced by the virus is being turned into a new generation of
virii the cell's hijacked replication machinery, so the choice of
host cell may make some difference.

Sadly for your credibility there are no "orders of magnitude"
differences on offer - that all comes from your over-active and
under-informed imagination.

James (Chicken Little) Arthur

You can considerably speed up virus mutations by infecting
cells with multiple viruses. The new generation of virii
easily incorporates bits of foreign NA, possibly picking up
new talents in doing so. While in nature this happens only
by chance, in the lab this can be arranged on purpose, and
with specific targets in mind. That's a far cry from random
mutation.

Jeroen Belleman
 
On Wednesday, August 6, 2014 2:17:53 PM UTC-4, k...@attt.bizz wrote:
On Wed, 6 Aug 2014 10:45:31 -0700 (PDT),

bloggs.fredbloggs.fred@gmail.com wrote:



On Wednesday, August 6, 2014 1:30:41 PM UTC-4, k...@attt.bizz wrote:





All of them? GMAFB!





It's always you worthless people



You're talking in a mirror, Blobbs.



who are so in fear of their life...



You're a liar, but everyone knows that already.

What everyone knows is you're a simple minded pest of no value whatsoever...
 
On Wed, 06 Aug 2014 08:22:52 +0200, David Brown
<david.brown@hesbynett.no> wrote:

On 06/08/14 00:38, krw@attt.bizz wrote:
On Mon, 4 Aug 2014 19:35:40 -0700 (PDT), dagmargoodboat@yahoo.com
wrote:

On Monday, August 4, 2014 6:50:29 PM UTC-4, k...@attt.bizz wrote:
On Mon, 4 Aug 2014 14:09:25 -0700 (PDT), dagmargoo...@yahoo.com wrote:
On Monday, August 4, 2014 4:56:47 PM UTC-4, bloggs.fred...@gmail.com wrote:
On Monday, August 4, 2014 4:45:31 PM UTC-4, dagmarg...@yahoo.com wrote:

http://abcnews.go.com/Health/WorldNews/ebola-stricken-american-doctor-turn-worse/story?id=24791024

That story is old and inaccurate. Originally he wanted the female to get the serum because he seemed better off. Then his condition rapidly deteriorated and they gave him the serum first.

Yep. Thanks for the correction.

The news was just reporting that both had received two doses of the
serum. The first didn't do much but the second made a big difference
in both. Dr. Brandtly reportedly walked (with help) from the
ambulance into the hospital and she was now well enough to fly (should
be here tomorrow).

I'm not worried about transmission--you've pretty well got to touch someone
to get it--but for people who worry...the serum came from San Diego.

The two doctors worked in full hazmat gear. How did they get it?
There is a lot that's not being said, here.

Haven't you seen "Outbreak"? Even with full hazmat gear, accidents can
happen.

A hundred times? Exactly what was the failure. I know "trust us, we
know better" is the phrase all statists use.

Actually, the ebola health care workers in Africa do not wear "full
hazmat gear" (as used in biolabs) - it would be impossible to work in in
that environment. They mostly wear masks, glasses, coveralls, gloves
and boots. The chances of ebola virus particles getting in somewhere
along the line (including the process of taking the cloths off at the
end of the shift) are small, but not negligible.

You're wrong. They had every inch of their bodies covered. The only
thing they didn't have is a separate oxygen system. These aren't the
only two to become infected. There is something not understood here.

So basically they were unlucky - there is no need (at this stage) to
worry that there is some unknown transmission vector.

All of them? GMAFB!

So, they've got virus too. Maybe that Spanish flu professor in
Minnesota can get in the game and make a super-er influbola bug.

Sounds about par.
 
On Wed, 6 Aug 2014 10:45:31 -0700 (PDT),
bloggs.fredbloggs.fred@gmail.com wrote:

On Wednesday, August 6, 2014 1:30:41 PM UTC-4, k...@attt.bizz wrote:


All of them? GMAFB!


It's always you worthless people

You're talking in a mirror, Blobbs.

>who are so in fear of their life...

You're a liar, but everyone knows that already.
 
On Thursday, 7 August 2014 10:12:24 UTC+10, k...@attt.bizz wrote:
On Wed, 6 Aug 2014 12:27:13 -0700 (PDT),
bloggs.fredbloggs.fred@gmail.com wrote:
On Wednesday, August 6, 2014 2:17:53 PM UTC-4, k...@attt.bizz wrote:
On Wed, 6 Aug 2014 10:45:31 -0700 (PDT),
bloggs.fredbloggs.fred@gmail.com wrote:
On Wednesday, August 6, 2014 1:30:41 PM UTC-4, k...@attt.bizz wrote:

All of them? GMAFB!

It's always you worthless people

You're talking in a mirror, Blobbs.

who are so in fear of their life...

You're a liar, but everyone knows that already.

What we all know is that krw thinks that anybody who disagrees with him has to be wrong, has to conscious that they are wrong, and thus maliciously lying.

Somebody a little smarter than krw might realise that this often isn't true.

What everyone knows is you're a simple minded pest of no value whatsoever...

You aren't smart enough to stop digging.

But he was smart enough to characterise krw precisely correctly, and we all know that krw isn't smart enough to entertain the possibility that Fred Bloggs might be right.

--
Bill Sloman, Sydney
 
On Wednesday, August 6, 2014 8:20:58 PM UTC-4, rickman wrote:

.... In fact one of the coping mechanisms of the cell is on

detecting an infection, to commit suicide before the virus has much

chance to replicate.

Ummm, no. There is a cell destruction known as apoptosis. I suppose it could be called a suicide because the cell thoroughly deconstructs itself to the point of shredding it own nuclear DNA. But this process is initiated by an enzyme injected into the cell cytoplasm by a killer T-lymphocyte. The killer lymphocyte detects an infected cell by recognizing a protein on the cell membrane the pathogen uses to gain entry to it. This is not a "coping" mechanism, it is another layer to the immune response carried out by the big guns, T-lymphocytes; it's also the last layer of the body's defense.
 
On Thursday, 7 August 2014 10:20:58 UTC+10, rickman wrote:
On 8/6/2014 12:30 PM, Bill Sloman wrote:
On Thursday, 7 August 2014 01:13:39 UTC+10, Jeroen Belleman wrote:

You can considerably speed up virus mutations by infecting cells with multiple viruses. The new generation of virii easily incorporates bits of foreign NA, possibly picking up new talents in doing so. While in nature this happens only by chance, in the lab this can be arranged on purpose, and with specific targets in mind. That's a far cry from random mutation.

Perhaps. Multiple viruses hitting the cell all at once are all going to be trying to take over the cells replicating machinery at the same time. The likeliest outcome is a very dead cell and no new viruses. You may be lucky and get a surviving hybrid, but you'd have to be very lucky to get one that could take over another cell and produce copies of itself.

Your idea of how a cell works and how viruses work is a bit simplistic.... or maybe I should say a bit too involved. The inter-cellular machinery that produces protein and copies NA is rather straight forward. You just shove your blueprints into the replicator and they get made. The final assembly of viruses is often automatic, for example they found that adding tobacco mosaic virus RNA with its protein coat results in the spontaneous creation of complete viruses.

Don't think this has to be a very efficient process either. Viruses are r-selected which means they will reproduce as many offspring as possible without much regard to the quality. Viruses use the machinery of a cell to produce many more viruses and disperse these viruses by rupturing the cell spew out the contents which includes many partially assembled
viruses and a lot of virus components. The cell pretty much always dies that I know of. In fact one of the coping mechanisms of the cell is on detecting an infection, to commit suicide before the virus has much chance to replicate.

The upshot of all this is that infection with multiple virus types does
not do any more damage to the cell than would otherwise happen and the two viruses have little impact on one another other than competing for the same machinery. So it is very easy for two virus types to share NA
if they infect the same cell.

The cell's replication machinery is making at least two independent virus components - the protein shell and the genetic material. In some viruses the genetic material is split into two or more separate components.

If we are talking about different strains of a flu virus, the protein shell will be more or less the same, but it's unlikely to exactly suit the genetic material from the other strain. If the genetic material is split up, the chance of the randomly assembled bits from two or more viruses coming together right is further reduced. The cell may not die much faster from a multiple infection, but it's replication machinery isn't going to work as well for either of the infecting agents.

Producing one that was as viable as the flu virus would be an even longer stretch.

And that is what evolution is all about. It can take millions and even billions of rolls of the dice to get a combination that is an
improvement, but the viruses have lots of time and replicate very, very quickly in huge numbers.

Correct. Which is why James Arthur's "hyper-accelerated artificially-directed human-targeted viral evolution" is such a load of alarmist rubbish.

> BTW, given that each time a person is infected it is like inoculating a petri dish, the natural process can result in some very fast mutations. There are a lot of petri dishes out there. In the lab not so many.

In the lab the viruses that get to survive, replicate and mutate can be selected - to some extent. In wild the capacity to replicate and get dispersed is the only criterion. In the lab the researchers can concentrate on the more lethal variants (if they've worked out what makes them lethal - looking at the recovered Spanish flu virus and the H7N9 chicken flu virus gives them clues about that).

In the wild a lethal flu virus is at a mild disadvantage - its hosts die and stop getting around to infect other people before their immune systems have stopped cells getting infected and churning out copies. It's a mild disadvantage because most of the propagation is done in the early stages of the infection.

--
Bill Sloman, Sydney
 

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