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PostPosted: Sun Apr 25, 2010 12:58 pm 
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lol,

the recombination clique (well, that's you and ....) might take over

cause for concern

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PostPosted: Sun Apr 25, 2010 1:51 pm 
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gsgs wrote:
lol,

the recombination clique (well, that's you and ....) might take over

cause for concern

It's not a might, but they will delay as long as possible. They really can't compete against the real data, and the propaganda is getting old.

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PostPosted: Sun Apr 25, 2010 10:13 pm 
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gsgs, are you really that certain that recombination doesn't exist?

I would really like to hear your thoughts concerning the physical mechanisms within a virus that would eliminate the possibility of recombination.


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PostPosted: Mon Apr 26, 2010 12:27 am 
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Pandora wrote:
gsgs, are you really that certain that recombination doesn't exist?

I would really like to hear your thoughts concerning the physical mechanisms within a virus that would eliminate the possibility of recombination.

I don't think you will hear much from GSGS on this area. It really becomes a VERY slippery slope VERY quickly. Homologous recombination is widely accepted for positive sense RNA virus (like coronaviruses or picornavirues). wo teh argument was that positive sense RNA could recombine, but negative (like flu) could not. Conceptually this makes no sense, because all viruses as well as all organisms with genes, need to make of double stranded version to survive (single stranded negative need to make a positive, while single stranded positive need to make a negative), and recombination is template dependent.

Moreover, a few years ago recombination was demonstrated for Ebola, which like flu is a single stranded negative sense virus, so the positive but not negative nonsense was experimentally shown to be utter nonsense.

When pressed, many of the deniers will more from "It can't happen" to "Even if it can happen its not important".

gsgs has stated that receombination does happen in flu, but is very rare becasue long stretches of divergent sequences are not found, which of course ignores the fact that most recombination will be between very closely related sequence because those of the types of combinations likely to be in the same host at the same time, and closely related sequence allow for a nascent RNA to jump from one template to another, because almost all regions on the new chain will have an idetical location to reanneal. Thus, you would expect to see exactly what you do see.

Therefore, I don't expect to see anything reasonal from gsgs, otehr thanhis perceptions of what other scientists think (and those linked by the influenza propagada are VERY threatened by recombination, which would have a VERY negative impact on their carreers because they have been telling anyone who would listen that there is no recombination in influenza and evolution can't be predicted (and like gssg, they have been saying this for YEARS and coming up with utter nonsesene, like only positive sense can recombine, or that D225G is spontaneous).

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PostPosted: Mon Apr 26, 2010 12:38 am 
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niman wrote:
Pandora wrote:
gsgs, are you really that certain that recombination doesn't exist?

I would really like to hear your thoughts concerning the physical mechanisms within a virus that would eliminate the possibility of recombination.

I don't think you will hear much from GSGS on this area. It really becomes a VERY slippery slope VERY quickly. Homologous recombination is widely accepted for positive sense RNA virus (like coronaviruses or picornavirues). wo teh argument was that positive sense RNA could recombine, but negative (like flu) could not. Conceptually this makes no sense, because all viruses as well as all organisms with genes, need to make of double stranded version to survive (single stranded negative need to make a positive, while single stranded positive need to make a negative), and recombination is template dependent.

Moreover, a few years ago recombination was demonstrated for Ebola, which like flu is a single stranded negative sense virus, so the positive but not negative nonsense was experimentally shown to be utter nonsense.

When pressed, many of the deniers will more from "It can't happen" to "Even if it can happen its not important".

gsgs has stated that receombination does happen in flu, but is very rare becasue long stretches of divergent sequences are not found, which of course ignores the fact that most recombination will be between very closely related sequence because those of the types of combinations likely to be in the same host at the same time, and closely related sequence allow for a nascent RNA to jump from one template to another, because almost all regions on the new chain will have an idetical location to reanneal. Thus, you would expect to see exactly what you do see.

Therefore, I don't expect to see anything reasonal from gsgs, otehr thanhis perceptions of what other scientists think (and those linked by the influenza propagada are VERY threatened by recombination, which would have a VERY negative impact on their carreers because they have been telling anyone who would listen that there is no recombination in influenza and evolution can't be predicted (and like gssg, they have been saying this for YEARS and coming up with utter nonsesene, like only positive sense can recombine, or that D225G is spontaneous).

In case you think the negative sense argument is too bizarre to be believed, here is the ProMED commentary by MP:

[The influenza viruses are negative-strand RNA viruses, and, as such, lack
the ability to interact by intermolecular recombination........
http://www.promedmail.org/pls/apex/f?p= ... ID:X,28016
Archive Number 20050207.0415
Published Date 07-FEB-2005
Subject PRO/AH> Avian influenza, poultry vaccines - China


AVIAN INFLUENZA, POULTRY VACCINES - CHINA
*****************************************
A ProMED-mail post
<http://www.promedmail.org>

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PostPosted: Mon Apr 26, 2010 12:47 am 
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To be fair to ProMED, when I searched recombination and H5N1 I found several more recent ProMED reports that acknowledge recombination as a mechanism or genetic evolution in influenza, and do so while also citing reassortment, leaving little doubt that they are talking about homologous recombination, and not just called reassortment recombination.

Recombination and sequences are not ProMED's strong suits and many times they just repeat nonsense fed to them by WHO consultants and the nonsense about negative sense RNA used to be widely cited by WHO consultants.

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PostPosted: Mon Apr 26, 2010 3:48 am 
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yes, recombination does happen. My list of possible/probable
examples/candidates is here:
http://www.setbb.com/fluwiki2/viewtopic ... m=fluwiki2

Shall all those examples be created in the laboratory, be sequencing errors ?
That looks unlikely. And, when it can happen in the lab while
growing the virus then why shouldn't happen it in nature too ?

What is a bit strange, though, is that we see no recombination
dynasties, survivors that generate decendants for years.
So an effect of recombination on the evolution of influenza has
not been demonstrated yet.
Other than with reassortment, which has clear and accepted effects
on evolution and which also requires double-infection
of a cell with 2 different viruses.

Niman goes even a step further, he claims that many/most of the
single-nucleotide-mutations that we see are due to coinfection
and recombinations. This is generally not accepted.
The best example for this that I'm aware of is the Ontario
genome from the genbank-thread. Again we have no descendants
of that virus.

Even with those few examples I think it's rare (rarer than reassortments
changing just one polymorphism) and most of his
"jumping polymorphisms" are IMO not due to recombination.

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PostPosted: Mon Apr 26, 2010 4:04 am 
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let me add, that recombination in human-flu is much rarer
than in birds or swine. See above linked list of candidates
or this thread for a more complete analysis:
http://www.flutrackers.com/forum/showth ... p?p=148571

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PostPosted: Mon Apr 26, 2010 4:33 am 
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gsgs wrote:
let me add, that recombination in human-flu is much rarer
than in birds or swine. See above linked list of candidates
or this thread for a more complete analysis:
http://www.flutrackers.com/forum/showth ... p?p=148571

In humans, dual infections with closely related sequences are more common, leading to short seqments like H274Y, which has already become fixed in seasonal H1N1 in patients not taking Tamiflu. The human examples in seasonal flu have been described in detail, including doubles and triples

http://precedings.nature.com/documents/2832/version/1

You have never address this daata, which is quite real, and H274Y was quite fixed in seasonal H1N1, before it was replaced with pH1N1, and as seen in sequences from Japan and South Korea, will soon be fixed in pandmeic H1N1, no reassortment required,

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PostPosted: Mon Apr 26, 2010 4:55 am 
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gsgs wrote:
yes, recombination does happen. My list of possible/probable
examples/candidates is here:
http://www.setbb.com/fluwiki2/viewtopic ... m=fluwiki2

Shall all those examples be created in the laboratory, be sequencing errors ?
That looks unlikely. And, when it can happen in the lab while
growing the virus then why shouldn't happen it in nature too ?

What is a bit strange, though, is that we see no recombination
dynasties, survivors that generate decendants for years.
So an effect of recombination on the evolution of influenza has
not been demonstrated yet.
Other than with reassortment, which has clear and accepted effects
on evolution and which also requires double-infection
of a cell with 2 different viruses.

Niman goes even a step further, he claims that many/most of the
single-nucleotide-mutations that we see are due to coinfection
and recombinations. This is generally not accepted.
The best example for this that I'm aware of is the Ontario
genome from the genbank-thread. Again we have no descendants
of that virus.

Even with those few examples I think it's rare (rarer than reassortments
changing just one polymorphism) and most of his
"jumping polymorphisms" are IMO not due to recombination.

Your comments on "jumping polymorphisms" are clearly your OPINION, which has nothing to do with the data or the concept of recombination. Your position that the rare and unlikely examples are due to recombination, but SNPs (single nucleotide polymorphisms) are not, lacks any logic. It's on a par with your suggestion that seasonal flu was fixing H274Y because of "traveling salesmen", or posts in June of 2009 that there was a 10-20% chance that the 2009 pandemic was not a pandemic. These opinions have no scientific or logical basis, and are the equivalent of saying the earth is flat because the the maps of the earth are flat.

Your own table on the polymorphisms in the 3 BP deletion sub-clade have clear examples of recombination. Your really don't understand patterns or clustering in time and space. The earlier example of G743A in H5N1, which was on multiple sub-clades in Egypt, as well as clades in Russia, Kuwait, Ghana, and Nigeria, and suddenly appeared in early 2007 is an example that can't be explained by random mutation or lab error, so you call it a "special case", and once again, you give no reason as to why it is "special".

http://precedings.nature.com/documents/459/version/3

Thus, you have the difficult examples you say are due to recombination, as well as the simple cases, which you can't explain, but say the thousands of other examples are "coincidences" like the 3 BP deletion itself, which is present on three VERY different H5N1 genetic backgrounds, and the unpublished sequences have the adjacent polymorphism I147T, which is in all Egyptian sequneces with 125del.

However, your own table has clear examples. One polymorphism is only found in two isoaltes in the entire Genbank datbase, yet both are in H5N1, clade 2.2, Egypt, the 125del sub-clade, in close proximity, and in samples collected within several weeks of each other. This type of clustrering in time and space destroys "random mutations", which can't explain why there are such unlikely "coicidences". Moreover, the same two subclades have the adjacent polymorphism when encodes A189T, creating another time and space problem for "random mutation" becasue it is rare, yet found clustered in the 125del subclade in sampels that are geographically close to each other which were colelcted in the same time frame.

This clustering is a death blow to "random mutation" which is why WHO put out its D225G "analysis". aka propaganda, for pandemic H1N1 in late December, 2009, because they knew that the Ukraine sequences would destroy their "random mutation" working hypothesis because D225G was clusered in time and space in Ukraine and Russia. In the Duke cluster it was even more problematic because of obvious transmission, so they tried the "lab error" route. which is utter nonense, since D225G was isoalted from two independent samples from the index case.

You still have provided no rationale as to why rare chance encounters would generate genetic exchanges by recombination, but the much more common dual infections involving closely related species would not, and the closely related recombination would produce single nucleotide polymorphisms. You are saying that a tree falling in the forest makes no sound if no one is listening. The explosion of sequences produces the clear time and space clustering that leaves no doubt that recombination leads to teh exchanges of single nucleotide polymorphisms.

The "look at the maps" explanation got VERY or VERY quickly years ago,

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