• FluTrackers.com Inc. does not provide medical advice. Information on this web site is collected from various internet resources, and the FluTrackers board of directors makes no warranty to the safety, efficacy, correctness or completeness of the information posted on this site by any author or poster. The information collated here is for instructional and/or discussion purposes only and is NOT intended to diagnose or treat any disease, illness, or other medical condition. Every individual reader or poster should seek advice from their personal physician/healthcare practitioner before considering or using any interventions that are discussed on this website. By continuing to access this website you agree to consult your personal physican before using any interventions posted on this website, and you agree to hold harmless FluTrackers.com Inc., the board of directors, the members, and all authors and posters for any effects from use of any medication, supplement, vitamin or other substance, device, intervention, etc. mentioned in posts on this website, or other internet venues referenced in posts on this website.
  • We are not asking for any donations. Do not donate to any entity who says they are raising funds for us.

(almost) no recombination in flu-B

Re: (almost) no recombination in flu-B

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:)
 
Re: (almost) no recombination in flu-B

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).

The recombination is quite real.
 
Re: (almost) no recombination in flu-B

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)
 
Re: (almost) no recombination in flu-B

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).
 
Re: (almost) no recombination in flu-B

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.
 
Re: (almost) no recombination in flu-B

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.
 
Re: (almost) no recombination in flu-B

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.
 
Re: (almost) no recombination in flu-B

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.

Thany you.
 
Re: (almost) no recombination in flu-B

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.
 
Re: (almost) no recombination in flu-B

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).

http://precedings.nature.com/documents/459/version/4

G743A is a dramatic example, but acquistions of SNPs are VERY common.

Another examples is H274Y in human H1N1, which has now appeared on Clade 1, 2B, and 2C genetic backgrounds (in the absence of oseltamivir).

Acquistion of SNPs via homologous recombination is the main driver of influenza evolution.

The "lab contamination" nonsense can only be used a few times. It gets very old very fast.

I will be using both examples in talks in Beijing in a few weeks

http://www.iddst.com/iddst2008/

http://www.recombinomics.com/presentations.html
 
Re: (almost) no recombination in flu-B

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.
 
Re: (almost) no recombination in flu-B

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).

http://precedings.nature.com/documents/459/version/4

G743A is a dramatic example, but acquistions of SNPs are VERY common.

Another examples is H274Y in human H1N1, which has now appeared on Clade 1, 2B, and 2C genetic backgrounds (in the absence of oseltamivir).

Acquistion of SNPs via homologous recombination is the main driver of influenza evolution.

The "lab contamination" nonsense can only be used a few times. It gets very old very fast.

I will be using both examples in talks in Beijing in a few weeks

http://www.iddst.com/iddst2008/

http://www.recombinomics.com/presentations.html

It can be explained by random mutation. However, I think it is a good example to detect positive selection in influenza virus.
 
Re: (almost) no recombination in flu-B

It can be explained by random mutation. However, I think it is a good example to detect positive selection in influenza virus.
No it can't. G743A is silent and appeared on multiple genetic backgrounds.

Each of these backgrounds picked up 2-6 changes and one was G743A and they all happened at the same time. Random mutation / selection doesn't explain this, which is why I use it as an example. Most of the time the data is not quite this dramatic, but I use G743A to eliminate the error/selection argument (but as noted above, it is still cited).

The random muttaion / selection mantra also gets very old very fast.
 
Re: (almost) no recombination in flu-B

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.

However, there are no acceptable model in published peer-review materials. It is impossible to detect recombination between very similar sequences, though there are thousands of handreds of recombination detection methods.
 
Re: (almost) no recombination in flu-B

However, there are no acceptable model in published peer-review materials. It is impossible to detect recombination between very similar sequences, though there are thousands of handreds of recombination detection methods.
G743A is an example of the "impossible".
 
Re: (almost) no recombination in flu-B

maybe some constraint makes G743A more likely, so it appears
independently on similar backgrounds

or mixed viruses, some with G743, some with A743 in the same
droplet


why SNPs but no double-NPs , triple... via recombination ?
 
Back
Top