OT: Gov wants to kill us..

[Bill Sloman]

On Thursday, 7 August 2014 11:10:26 UTC+10, k...@attt.bizz wrote:

On Wed, 6 Aug 2014 17:48:05 -0700 (PDT), Bill Sloman
bill.sloman@gmail.com> wrote:
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.

Yeah, here comes Slowman to take his turn shoveling. You really are a
dummy, Slowman.

Not exactly. You think that I'm a dummy, which is just one more of your foolish delusions. Put forward enough counter-factual opinions and people get to realise that your opinions are worthless. You won't, but your quality control criterion is whether an opinion agrees with yours, as opposed to objectively established facts.

--
Bill Sloman, Sydney

 

On Wednesday, August 6, 2014 9:14:53 PM UTC-4, Bill Sloman wrote:

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

Interestingly about 8% of the human genome is provirus, which is A LOT. That is virus DNA integrated into nuclear DNA and frozen there, no further replication. And this stuff is heritable, passed down to subsequent generations.
http://en.wikipedia.org/wiki/Provirus

 

On Wednesday, August 6, 2014 10:01:07 PM UTC-4, rickman wrote:

On 8/6/2014 8:55 PM, bloggs.fredbloggs.fred@gmail.com wrote:

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.



Bloggs, what is your point? I was showing that your statement,

"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. " is not

valid. Do you have a response to that?

My response is I never made that statement. Multiple virus infection of a single cell is called superinfection and has been observed for nearly 70 years now. The outcome depends on the viruses and the host cell.

--



Rick

 

On Wednesday, August 6, 2014 10:21:10 PM UTC-4, rickman wrote:

It can be more than a "mild" disadvantage. It depends on the nature of

transmission and the extent of the impact. Most diseases on reaching a

pandemic status have already started to mitigate their virulence. If I

remember correctly the bubonic plague was less lethal each of the

several times it covered Europe.

That plague was a bacteria, not a virus. Now the maniacs are saying it was actually ebola. This ebola hysteria is something else, like now is the perfect time to bring this up:

http://www.nytimes.com/2001/10/02/science/new-theories-link-black-death-to-ebola-like-virus.html

--



Rick

 

[Bill Sloman]

On Thursday, 7 August 2014 12:21:10 UTC+10, rickman wrote:

On 8/6/2014 9:14 PM, Bill Sloman wrote:
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.

You actually don't know anything about this and are making all this up,

Wrong.

Look up r-selection for species and learn about reproduction
techniques. The effect you are talking about is not very significant.

Everybody knows about reproductive strategies. It would be a very unusual virus which could opt for any strategy except maximising the number of of it's off-spring. Viruses aren't really equipped to modify the environment their off-spring are exposed to.

This process only has to produce one new virus that ultimately infects
another cell and begins multiplying.

It's got to produce a lot more than one to have any significant chance of producing an off-spring that can get to cell it can infect.

> We aren't talking about the mainstream method of propagation for the new virus, just how one can be created.

But the chance of the new virus getting a chance to propagate also gets into the calculation.

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.

It can be more than a "mild" disadvantage. It depends on the nature of transmission and the extent of the impact. Most diseases on reaching a pandemic status have already started to mitigate their virulence. If I remember correctly the bubonic plague was less lethal each of the several times it covered Europe.

The human population had also been selected by the process. Apparently there's a human gene variant that provides protection against AIDS which is more common in people whose ancestors survived close encounters with the bubonic plague (as in relatives dying of it).

The first outbreak of the plague killed off about 30% of the population.All three of the Limburg Brothers - famous medieval artists who came from Nijmegen (which is how I got to hear about them) all died in the same outbreak. That family clearly got selected out.

http://en.wikipedia.org/wiki/Limbourg_brothers

--
Bill Sloman, Sydney

 

[Bill Sloman]

On Thursday, 7 August 2014 12:01:07 UTC+10, rickman wrote:

On 8/6/2014 8:55 PM, bloggs.fredbloggs.fred@gmail.com wrote:
On Wednesday, August 6, 2014 8:20:58 PM UTC-4, rickman wrote:

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

Bloggs, what is your point? I was showing that your statement, "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. " is not valid.. Do you have a response to that?

It wasn't his statement, but mine. And my response is that since your counter-argument consists of a statement that one the less likely outcomes - some mixed up viruses - is still likely enough to be significant, you can scarcely use that as a basis for claiming that the part of my statement that you have quoted isn't valid.

I did go on to observe that a mixed virus was one of the less likely potential outcomes, so what we are in fact arguing about is the numerical weight you should attach to "likely" and "less likely".

--
Bill Sloman, Sydney

 

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

You aren't smart enough to stop digging.

 

[rickman]

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.


> 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.

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.

--

Rick

 

On Wed, 6 Aug 2014 17:48:05 -0700 (PDT), Bill Sloman
<bill.sloman@gmail.com> wrote:

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.

Yeah, here comes Slowman to take his turn shoveling. You really are a
dummy, Slowman.

 

[rickman]

On 8/6/2014 9:14 PM, Bill Sloman wrote:

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.

You actually don't know anything about this and are making all this up,
no? Look up r-selection for species and learn about reproduction
techniques. The effect you are talking about is not very significant.
This process only has to produce one new virus that ultimately infects
another cell and begins multiplying. We aren't talking about the
mainstream method of propagation for the new virus, just how one can be
created.

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.

It can be more than a "mild" disadvantage. It depends on the nature of
transmission and the extent of the impact. Most diseases on reaching a
pandemic status have already started to mitigate their virulence. If I
remember correctly the bubonic plague was less lethal each of the
several times it covered Europe.

--

Rick

 

[rickman]

On 8/6/2014 9:46 PM, bloggs.fredbloggs.fred@gmail.com wrote:

Interestingly about 8% of the human genome is provirus, which is A LOT. That is virus DNA integrated into nuclear DNA and frozen there, no further replication. And this stuff is heritable, passed down to subsequent generations.
http://en.wikipedia.org/wiki/Provirus

Only if the somatic cells are infected. Interesting to note that only
about 2% of the human genome is used to code for proteins.

--

Rick

 

[rickman]

On 8/6/2014 8:55 PM, bloggs.fredbloggs.fred@gmail.com wrote:

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.

Bloggs, what is your point? I was showing that your statement,
"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. " is not
valid. Do you have a response to that?

--

Rick

 

[rickman]

On 8/6/2014 11:46 PM, Bill Sloman wrote:

On Thursday, 7 August 2014 12:01:07 UTC+10, rickman wrote:
On 8/6/2014 8:55 PM, bloggs.fredbloggs.fred@gmail.com wrote:
On Wednesday, August 6, 2014 8:20:58 PM UTC-4, rickman wrote:

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

Bloggs, what is your point? I was showing that your statement, "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. " is not valid.. Do you have a response to that?

It wasn't his statement, but mine. And my response is that since your counter-argument consists of a statement that one the less likely outcomes - some mixed up viruses - is still likely enough to be significant, you can scarcely use that as a basis for claiming that the part of my statement that you have quoted isn't valid.

I did go on to observe that a mixed virus was one of the less likely potential outcomes, so what we are in fact arguing about is the numerical weight you should attach to "likely" and "less likely".

Who are you, George Bush Sr? "no new viruses" BUSTED!

--

Rick

 

[Bill Sloman]

On Thursday, 7 August 2014 13:55:12 UTC+10, rickman wrote:

On 8/6/2014 11:46 PM, Bill Sloman wrote:
On Thursday, 7 August 2014 12:01:07 UTC+10, rickman wrote:
On 8/6/2014 8:55 PM, bloggs.fredbloggs.fred@gmail.com wrote:
On Wednesday, August 6, 2014 8:20:58 PM UTC-4, rickman wrote:

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

Bloggs, what is your point? I was showing that your statement, "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. " is not valid.. Do you have a response to that?

It wasn't his statement, but mine. And my response is that since your counter-argument consists of a statement that one the less likely outcomes - some mixed up viruses - is still likely enough to be significant, you can scarcely use that as a basis for claiming that the part of my statement that you have quoted isn't valid.

I did go on to observe that a mixed virus was one of the less likely potential outcomes, so what we are in fact arguing about is the numerical weight you should attach to "likely" and "less likely".

Who are you, George Bush Sr? "no new viruses" BUSTED!

Since I failed to say "no new viruses" and in fact explicitly observed that they did get produced - if not very often - it's your stance that is busted, rather than mine.

Are you intentionally channeling James Arthur's pathetic strawman style of argument, in which case you earn satirist points, or are you just demonstrating that you can't process a statement that stretches over more than one sentence?

--
Bill Sloman, Sydney

 

On Wednesday, August 6, 2014 10:21:10 PM UTC-4, rickman wrote:

You actually don't know anything about this and are making all this up,

no? Look up r-selection for species and learn about reproduction

techniques. The effect you are talking about is not very significant.

This process only has to produce one new virus that ultimately infects

another cell and begins multiplying. We aren't talking about the

mainstream method of propagation for the new virus, just how one can be

created.

No such merging of /unrelated/ viruses has been observed.

"Many viruses (for example, influenza A virus) can "shuffle" their genes with other viruses when two similar strains infect the same cell. This phenomenon is called genetic shift, and is often the cause of new and more virulent strains appearing. Other viruses change more slowly as mutations in their genes gradually accumulate over time, a process known as genetic drift."

Since there is and always has been unlimited opportunity for something like this to occur, it cannot happen between unrelated strains.


See the article on evolutionary biology:
http://en.wikipedia.org/wiki/Viral_evolution