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,