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...homologous recombination in influenza B viruses was very rare or absent and could not confer a substantial fitness advantage. Therefore, we conclude that homologous recombination is unlikely to play a major role in influenza B virus evolution.
From this paper, we can fond that homologous recombination is rare, because the coinfection is common. Homologous recombination betweem similar sequences should be similar to recombination between diffent linkages. So the recombination claimed by Nilman seems to be nonsense. We live in a world anybody can say anything about anyone
From this paper, we can fond that homologous recombination is rare, because the coinfection is common. Homologous recombination betweem similar sequences should be similar to recombination between diffent linkages. So the recombination claimed by Nilman seems to be nonsense. We live in a world anybody can say anything about anyone
I haven't looked at influenza B, but there is no reason to think that recombination is limited to influenza A. The methods used by these groups have problems with short sequences, although Boni found high levels in NA sequences (p less that 1 in 10 billion).
however , influenza B is restricted to humans and I think, we agree that
recombination in humans is rarer than in birds or swine. (for flu-A)
No, we disagree. The OBVIOUS recombination is greater in influenza A, but I suspect influenza B is like influenza A with regard to recombination between closely related sequences, which is easily the most common form of homologous recombination (although most mistakenly assume these single nucleotide polymorphisms are due to recent copy errors).
Please. The coinfection of influenza B virus is common. If recombination between similar sequences occurs frequently, then recombination between viruses of different likages would be frequent. However, the fact is not. Although I think there are recombination events in influenza viruses, the rates should be low.
To date, it is difficult to use SNPs to detect the recombination, because you can not clarify which is which.
No, we disagree. The OBVIOUS recombination is greater in influenza A, but I suspect influenza B is like influenza A with regard to recombination between closely related sequences, which is easily the most common form of homologous recombination (although most mistakenly assume these single nucleotide polymorphisms are due to recent copy errors).
I think you guys shold note the mutation' contributions to the evolution of viruses. Althogh I do not have a profound knowlege of your method, the recombination between closely related sequences is unreliable.
when there is much obvious reassortment (full segments) and few
obvious recombination (~half segments) and no spreading
of obvious recombination, then I conclude that their role in
influenza evolution is small.
Please. The coinfection of influenza B virus is common. If recombination between similar sequences occurs frequently, then recombination between viruses of different likages would be frequent. However, the fact is not. Although I think there are recombination events in influenza viruses, the rates should be low.
To date, it is difficult to use SNPs to detect the recombination, because you can not clarify which is which.
when there is much obvious reassortment (full segments) and few
obvious recombination (~half segments) and no spreading
of obvious recombination, then I conclude that their role in
influenza evolution is small.
I quite agree with you. Homologous recombination paly a minor role in the evolution of influenza viruses. We also should pay attention to the contamination. The recombinants identified by Han et al. are reallly artifical mosaics.
Please. The coinfection of influenza B virus is common. If recombination between similar sequences occurs frequently, then recombination between viruses of different likages would be frequent. However, the fact is not. Although I think there are recombination events in influenza viruses, the rates should be low.
To date, it is difficult to use SNPs to detect the recombination, because you can not clarify which is which.
Actually, you can identify SNPs, but the analysis is difficult. The example I use that is informative is G743A in the NA of H5N1. At the beginning of 2007, it appeared in isolates representing multiple clade 2.2 backgrounds (in Russia, Kuwait, Egypt, Ghana, and Nigeria).
In Egypt isolates were plaque purified to eliminate confusion that could be linked to mixed infections and the same change happened simultaeously on two distinct genetic backgrounds (which were in circulation earlier without the acquistion).
Please. The coinfection of influenza B virus is common. If recombination between similar sequences occurs frequently, then recombination between viruses of different likages would be frequent. However, the fact is not. Although I think there are recombination events in influenza viruses, the rates should be low.
To date, it is difficult to use SNPs to detect the recombination, because you can not clarify which is which.
The recombination can be easily missed, because it happens many times and the result is usually a SNP or two (which you then call "random mutations"), because the most common recombination is between closely related sequences.
Actually, you can identify SNPs, but the analysis is difficult. The example I use that is informative is G743A in the NA of H5N1. At the beginning of 2007, it appeared in isolates representing multiple clade 2.2 backgrounds (in Russia, Kuwait, Egypt, Ghana, and Nigeria).
In Egypt isolates were plaque purified to eliminate confusion that could be linked to mixed infections and the same change happened simultaeously on two distinct genetic backgrounds (which were in circulation earlier without the acquistion).
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