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Recombination possibility - My Question to Niman in sequences lingo...
Re: Recombination possibility - My Question to Niman in sequences lingo...
The change is silent in the NP gene.
So it can spread in every NP gene of every strain without consequences.
But it can give to a H5N1 strain a built-in ability to recombine from his own inside gene without the need of a dual infection for a a-2,3 to a-2,6 affinity switch if this segment recombine from the NP to the HA gene.
I'm sure you'll have no problem to see what change it could cause in the HA.
So now...
Is it possible ?
Last edited by Mingus; October 17, 2006, 12:37 PM.
Institut fur Virologie, Justus-Liebig-Universitat Giessen, Germany.
Mutants of the influenza virus A/seal/Mass/1/80 (H7N7) are described which contain an insertion of 60 nucleotides in the hemagglutinin (HA) gene, derived most probably by recombination between the HA gene and the nucleoprotein gene of the same virus. The nonhomologous RNA recombination resulted in an enhanced hemagglutinin cleavability associated with broadening of the host cell spectrum, increased hemolytic activity, and increased pathogenicity for chickens.
PMID: 8091680 [PubMed - indexed for MEDLINE]
</dd><dd class="links" id="links8091680">Related Links
Re: Recombination possibility - My Question to Niman in sequences lingo...
Originally posted by niman
You can get lots of gene crosses if the sequence is short enough.
I would not consider silent changes to be without consequences. The thrid base transitions are NOT random.
I know, I know this is not random.
But I mean the NP gene of americans Dog's H3N8 is highly similar to the NP gene of the Quigai strains or any H5N1 strains & recombination NP to NP is very frequent & plausible in a dual infection.
Also, because the A->T change in the AACGGGCA(T)A section is silent, there will have no selective pressure on it ( no repercussion on the protein )
So this polymorphism can spread in a H5N1 strain if H5N1 & H3N8 met each other here in america.
Since the time a H5N1 have this AACGGGCTA section in his NP gene, there will have an internal recombination risk with the H5 gene.
There will be no need for a dual infection, the donnor & the acceptor will be there in every cells.
Thanks Sonny, that was exactly the article who gave me this kind of Idea.
The H5 gene with AACGGGCTA instead of AACGGGCAA will code for L226 instead of Q226; this one will not be a silent change.
This recombination result could not be amplify if there is no selective pressure on it ( while the virus is in birds ) but could be there to happen opportunistically when the virus is replicating in human or in mammals ( positive selective pressure )
So again Dr.Niman, is it possible ?
Is there a constraint in your recombination laws that go against this possibility ?
Re: Recombination possibility - My Question to Niman in sequences lingo...
Originally posted by Mingus
I know, I know this is not random.
But I mean the NP gene of americans Dog's H3N8 is highly similar to the NP gene of the Quigai strains or any H5N1 strains & recombination NP to NP is very frequent & plausible in a dual infection.
Also, because the A->T change in the AACGGGCA(T)A section is silent, there will have no selective pressure on it ( no repercussion on the protein )
So this polymorphism can spread in a H5N1 strain if H5N1 & H3N8 met each other here in america.
Since the time a H5N1 have this AACGGGCTA section in his NP gene, there will have an internal recombination risk with the H5 gene.
There will be no need for a dual infection, the donnor & the acceptor will be there in every cells.
Thanks Sonny, that was exactly the article who gave me this kind of Idea.
The H5 gene with AACGGGCTA instead of AACGGGCAA will code for L226 instead of Q226; this one will not be a silent change.
This recombination result could not be amplify if there is no selective pressure on it ( while the virus is in birds ) but could be there to happen opportunistically when the virus is replicating in human or in mammals ( positive selective pressure )
So again Dr.Niman, is it possible ?
Is there a constraint in your recombination laws that go against this possibility ?
I have focused on stretches of 10 or more exact matches. It is possible that less can be used, but once the number gets too low, there will be many competing possibilities. Since flu is segemented, there could be jumping without dual infections, and there are small regions of identity on multiple genes, which could be involved in packaging.
Most acquired polymoprhisms however, can easily be found with the 10 BP minimum.
Re: Recombination possibility - My Question to Niman in sequences lingo...
Originally posted by niman
I have focused on stretches of 10 or more exact matches. It is possible that less can be used, but once the number gets too low, there will be many competing possibilities. Since flu is segemented, there could be jumping without dual infections, and there are small regions of identity on multiple genes, which could be involved in packaging.
Most acquired polymoprhisms however, can easily be found with the 10 BP minimum.
Thank you Dr.Niman, I take this as a yes.
So now, it would be interesting to monitor this section of the NP gene in H5N1 and to closely watch for dog's H3N8 signature.
You know, It would also produce an interesting experience in a laboratory that would bring conclusives proof of recombination in H5N1 to those who do not consider the idea.
A H5N1 strain with the (706C 708G 711T) segment in the NP gene sequence would give rise to a 226L in H5 protein in less MDCK cells passage than a regular H5N1 strain who may never achieve that. ( Due to the recombination possibility & the selective pressure in MDCK cells to amplify the new born in the mix )
A positive result would strongly support the copy-choice recombination theory.
A negative result would only suggest that the "rules" are more complex than expected.
Upon this gifted age, in its dark hour,
Rains from the sky a meteoric shower
Of facts....They lie unquestioned, uncombined.
Wisdom enough to leech us of our ill
Is daily spun, but there exists no loom
To weave it into fabric..
Edna St. Vincent Millay "Huntsman, What Quarry"
All my posts to this forum are for fair use and educational purposes only.
But for a single mutation Q226L, recombination with NP would
probably not
be required. We see a few such point-mutations in almost every human H5N1 isolate. And these mutations usually differ in different isolates.
So, considering the large amount of viruses in a host, I assume
that hundreds or thousands of single-point mutations are "tested"
in one infection. Most will be less viable, but if Q226L were more
viable, I think it has a good chance to evolve by "normal"
methods.
This may include short recombinations with NP or whatever,
which has the effect of just one nucleotide changing.
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