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 Post subject: Re: flu-A evolution
PostPosted: Wed Oct 14, 2009 2:03 pm 
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and here some direct evolution from ancestor virus to progeny:

Code:
equine H3N8,45 years: 62, 71, 72, 90, 62, 78, 38, 41   1963-2008
human  H3N2,35 years: 53, 65, 52,113, 62, 92, 42, 52  1972-2007
swine  H1N1,11 years: 29, 31, 33,---, 29,---,---, 34   1998-2009  mexflu
human  H1N1,64*years:105, 92, 91,154, 88,138, 74, 89  1918-2007 -25 years
human  H3N2,54 years: 97,---, 80,---, 87,---, 60, 83  1918-1972
human  H1N1,30 years: 53, 57, 51, 75, 44, 78, 39, 56   1977-2007
swine  H1N1,45 years: 75, 91, 72,109, 69,101, 61, 61   1931-1976
swine  H1N1,22 years: 60, 61, 68, 86, 59, 66, 59, 60    1981-2003  European swine

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Last edited by gsgs on Wed Oct 14, 2009 3:00 pm, edited 1 time in total.

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 Post subject: Re: flu-A evolution
PostPosted: Wed Oct 14, 2009 2:51 pm 
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gsgs wrote:
here is a list with some selected distances.
8 numbers for every pair of viruses telling their nucleotide-difference in the 8 segments in promille. NS is segment 8
... ...
and here some direct evolution from ancestor virus to progeny:

gsgs, thank you for the research grade work and valuable data! I really appreciate it!

I think I’ve got plenty of homework now!


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 Post subject: Re: flu-A evolution
PostPosted: Wed Oct 14, 2009 4:27 pm 
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Maybe on avian host NS1 function is different from mammals.
That could explain slower bird NS nucleotide substitution rates.
Here's an excerpt of a 2005 paper from Emergence of New Epidemic Viruses through Host Switching:

Quote:
The NS1 gene shows an evolutionary rate in human viruses which might indicate that it is
adapting to enhance viral replication. One of the best described functions of NS1 is as an
interferon antagonist. It is possible that avian virus NS1 genes do not function in this role
efficiently in the mammalian host
, perhaps due to inherent differences in innate immunity
between birds and mammals
. Indeed we have noted that mammalian cells deficient in the
interferon response become permissive to avian influenza strains. We assembled a panel
of avian and human influenza viruses and tested the extent to which they induced an
interferon response. In general the avian viruses induced more interferon than the human
viruses supporting the idea that an inability to counter interferon induction could limit
avian virus replication. However, the trait did not map genetically to the NS1 protein.
Moreover, we identified several human viruses which also induced high levels of
interferon. Some of those viruses were able to suppress the expression of newly
transcribed mRNAs, so that the interferon induced genes would not be expressed. In
contrast some of the avian strains were less able to suppress expression from the
interferon stimulated response element (ISRE). It may be that productive viral infection
is facilitated only when a temporal balance between virus and host cell is achieved in
which a sufficient level of viral gene expression is accumulated before host innate
immunity ‘kicks in’
.


PS: Are your table distances absolute or normalized (mutations/gene length)?
OK! (distance=1/100 % of nucleotides changed)


(3) Influenza virus : cell interactions,
Wendy Barclay
Emergence of New Epidemic Viruses through Host Switching
September 6-8, 2005 Steering Committee:
Colin Parish, Chairman Linda Saif, Charlie Calisher, Robert Webster, Donald Burke,Peter Daszak,
David Morens, Karen Lacourciere, Eun-Chung Park, Cristina Cassetti, Patricia Repik

http://www3.niaid.nih.gov/topics/viral/PDF/newepi_program.pdf


Last edited by neuromedia on Wed Oct 14, 2009 4:42 pm, edited 1 time in total.

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 Post subject: Re: flu-A evolution
PostPosted: Wed Oct 14, 2009 4:42 pm 
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normalized, difference in promille of availabe nucleotides

2280,2274,2151,1701,1497,1410,982,844 nucleotides in the 8 segments

I have more such tables, also with birds,
but they are often too big to post

we have 2 entirely different types of NS-segments.
Viruses should be called H1N1NS1 to account for this.
Most (~90%) are type 1, but many of the Alaska H3N8
birds are H3N8NS2

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 Post subject: Re: flu-A evolution
PostPosted: Thu Oct 15, 2009 2:20 am 
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interesting that NS has different tasks in birds vs. humans.
But can it be the reason for low mutation rates ? Most
mutations are synonymous.

Evolution in NS(segment 8) is slow especially in birds, not so much in humans.
Evolution in MP(segment 7) is slow in humans and birds.

But in birds there are some examples of particularly slow evolution
in other segments too, although not so many as in segments 7,8
It's difficult to determine in birds since segments mix (reassort)
frequently.

human:105, 92, 91,154, 88,138, 74, 89 (H1N1,1918-2007*)
swine:128,123,119,155,112,144, 80,117 (H1N1,1931-2006)
avian: 73,117,111,132, 89,131, 64, 67 (H5N1, 1959-2005)
avian: 95,103, 94,---, 75,111, 43, 40 (H51N1,1959-2003)
avian: 102, 85, 80,---,126,---, 52, 35 (H1N1,<1918-1968)

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 Post subject: Re: flu-A evolution
PostPosted: Thu Oct 29, 2009 10:22 am 
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gsgs wrote:
interesting that NS has different tasks in birds vs. humans.
But can it be the reason for low mutation rates ? Most
mutations are synonymous.

Evolution in NS(segment 8) is slow especially in birds, not so much in humans.
Evolution in M(segment 7) is slow in humans and birds.

But in birds there are some examples of particularly slow evolution
in other segments too, although not so many as in segments 7,8
It's difficult to determine in birds since segments mix (reassort)
frequently.

I noticed that evolution in NP (segment 5) is also slow in some examples of your list.
Is the S/N rate (Synonimous/Nonsynonimous) hight as well?
This could possibly signal that some genes are close to evolutionary stasis on birds?

There is a related discussion on the NP avian genes and 1918 sequences on the paper:
Novel Origin of the 1918 Pandemic Influenza Virus Nucleoprotein Gene
Ann H. Reid, Thomas G. Fanning, Thomas A. Janczewski, Raina M. Lourens, and Jeffery K. Taubenberger*
http://jvi.asm.org/cgi/content/full/78/22/12462


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 Post subject: Re: flu-A evolution
PostPosted: Thu Oct 29, 2009 11:00 am 
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I ignored amino-acid changes so far ...

maybe I can make a table later

-----------------------

I should have done this earlier

--------------------------


very interesting , amino-acid changes and nucleotide changes
seem to differ in NP(segment 5)
and presumably in others too
----edit---- also segment 1

more amino-acid-changes in humans (~twice), fewer in birds


--------------------------------

another confirmation that the 1918-virus is avian
give it 10 years in mammals or such, that doesn't really matter.
But it unlikely wasn't in mammals in 1889 (IMO)


--------------------
in segment 5 the early swine is closer to birds than the 1918 virus !
higher ratio of synonymous/nonsynonymous mutations

not so segment 1

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no patents on genes, publish the GISAID sequences !


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 Post subject: Re: flu-A evolution
PostPosted: Fri Oct 30, 2009 6:14 am 
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so, why does flu make much more amino-acid mutations
in the inner segments in mammals ovr the decades ?

Not so much on the nucleotide-level, so bird viruses
which are very distant on the nucleotide level are
still close on the amino-acid-level.
Even the South-American birds or Dk/LA/17G


and why didn't I see this question being asked before ?

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 Post subject: Re: flu-A evolution
PostPosted: Fri Oct 30, 2009 10:18 am 
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gsgs wrote:
and why didn't I see this question being asked before ?

Last question is the easier to answer:
I guess you are a natural born researcher! If so, from time to time, you reach a conclusion which sounds familiar to you.
You want to quote it and start wandering “where did I read that? I just can’t find the reference”.
A couple of days latter, you finnaly realize that you didn’t read it anywhere!. It was never written before!
The idea was conceiveid in your mind and sounded so familiar because of your long coexistence with the subject.

I guess this the reason you are wondering on questions never asked before. Perhaps it's still "Terra Incognita" everyone else!


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 Post subject: Re: flu-A evolution
PostPosted: Fri Oct 30, 2009 1:03 pm 
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this looks too important to have been missed


average ratio synonymous/nonsynonymous differences
in 5 chosen distant avian virus pairs (segments 1,2,3,5) = 6.22
(Brevig/1918 qualifies as avian here)

same for 4 mammalean flu-virus-pairs = 2.24

over 50-200 years



how to explain ?

is there less freedom/opportunity , more constrainsts for
flu-evolution in birds ? Many amino-acid changes
which are possible in mammals don't work in birds ?

Or is it just slower and takes longer in birds ?

In any case, there are limitations for flu-evolution
in birds which are not seen in mammals


only for the inner segments, HA and NA are different,
MP and NS have overlapping reading rames and are shorter

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