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What's on the genetic menu for New A/H1N1 and seasonal A/H1N1 & A/H3N2 swapping?

AlaskaDenise

AlaskaDenise

In Memoriam
There have been many references to what may/may not happen when this new A/H1N1 (swine origin) is circulating concurrently with seasonal A/H1N1 & A/H3N2 in the southern hemisphere during the coming months. If we can leave H5N1 out of this discussion and concentrate on circulating human influenza/A, what are the possible combinations?

By my count, I see:

from seasonal H1N1:
- PB2/E627K - sets the viral replication temperature to human upper respiratory conditions.
- NA/H274Y - blocks the success of neuraminidase-inhibtor antivirals (tamiflu)

from seasonal H3N2:
- M2/S31N - blocks the success of adamantane antivirals

Are there others?

What is the probability of the new H1N1 picking up any of the above, if not in the next 6 months, in any of the subsequent flu cycles? What is the impact?

I believe WHO is thinking of this situation in some of their statements.

.
 
Re: What's on the genetic menu for New A/H1N1 and seasonal A/H1N1 & A/H3N2 swapping?

logicalAmerican said:
Anything in NS? Didn't Dr Niman say that he was going to take a look? See http://www.flutrackers.com/forum/showthread.php?t=100274. Did he ever get back?
Click to expand...

Mamabird said the NS1/92 gene (the viral bullet-proof vest so it won't be killed by most of the human-immune-system ammunition) was okay! It's not in the other widely-circulating influenza/A.....so I left it out of this thread.

I believe that has only existed in (edited: 1918/H1N1=error) and current HP (high path) H5N1.

.
 
Last edited:
Re: What's on the genetic menu for New A/H1N1 and seasonal A/H1N1 & A/H3N2 swapping?

Since it is not in a widely circulated human influenza, I'd say the probability is lower than the others.

My purpose for this thread is to explore the more likely combinations that we may be dealing with in the next 6-12-18 months, rather than less likely worse case scenerios. I fear the current events may foster complacency and if we understand the likely future of this virus, we can maintain a realistic view of the situation.

.
 
Re: What's on the genetic menu for New A/H1N1 and seasonal A/H1N1 & A/H3N2 swapping?

We should also consider the opposite - what would be the result of A/H3N2 or seasonal A/H1N1 acquiring genes from swine A/H1N1?

Which H1N1 will come out the stronger? Old, new, which combination, or will we have 2 somewhat different circulating A/H1N1?

.
 
Re: What's on the genetic menu for New A/H1N1 and seasonal A/H1N1 & A/H3N2 swapping?

IOH has alerted us to the possibilty of a mixture with H9N2, a fairly-well humanized flu circulating in birds, with occasional human infections.

What pathogencity factors that will bring to the mix I'm not sure at this point.

His link:

Minimal molecular constraints for respiratory droplet transmission of an avian?human H9N2 influenza A virushttp://www.pnas.org/content/106/18/7565.short?rss=1

Thanks IOH.

.
 
Re: What's on the genetic menu for New A/H1N1 and seasonal A/H1N1 & A/H3N2 swapping?

Provided in 1, below are the problem amino acids associated with the currently circulating Swine Flu. These are generally found in every pandemic virus and most seasonal flu viruses, and some relate to sensitivity to antivirals, etc. All the available Swine Flu virus gene sequences have these human/problem characteristics.

1. PB2: A199S; PB1 N(T)375S; PB1-F2 P(R)48Q; PA T129I and S409N; HA E190D, S221P, F251L and Y258F; NP V33I, R100V and Q357K; MP K27R, I168T and N224S; M2 none; NS2 F55L; NA none.

Provided in 2, below are those amino acids that this bug has not yet obtained, but if obtained, could be problematic. Some are more important that others. None of the Swine Flu viruses have these characteristics as far as I know, but we should all keep an eye out for them>

2. PB2 L(F)475M, D567N and E627K; PB1 none; PB1-F2 P28L, D55N, I(V)100A and T552S; HA multi-basic amino acids at the clevage site (usually associated only with poultry infections); NP G16D, L283P and F313Y; MP I15V, K101R, A166V and N207S; M2 E16G and S20N; NS none; NS2 none; NA H274Y and N294S.

In other words, the Swine Flu virus has about half of the problem amino acids already in its tool box. The only other viruses even close to this are some H9N2 viruses circulating widely in Hong Kong and H7N7 in the Netherlands. As to the wild type avian viruses, only the North American variety come close.

Take away: This is a problem virus that bears watching closely. Reassortment with seasonal flu or H5N1 could be interesting.
 
Re: What's on the genetic menu for New A/H1N1 and seasonal A/H1N1 & A/H3N2 swapping?

This is a problem virus that bears watching closely
Click to expand...

Thankfully, you're hard at work doing just that. :applause:

That's a lot of variables to look for. It would seem that given all the possiblities and several viruses to pick from, the new H1N1 (swine) cannot avoid picking a few morsels from the menu.

The importance of sharing sequences between all countries is now quite obvious to the public (and MSM).

Thanks Mamabird for sharing your expertise.

.
 
Re: What's on the genetic menu for New A/H1N1 and seasonal A/H1N1 & A/H3N2 swapping?





INFLUENZA A (H1N1) - WORLDWIDE (11): COINCIDENT H3N2 VARIATION


Date: Tue 5 May 2009 12:08:07 -0700
From: Danuta Skowronski
<Danuta.Skowronski@bccdc.ca>


Recent mutations away from the 2008-09 influenza vaccine strain among
North American A/H3N2 virus coincident with emergence of novel A/H1N1
--------------------------------------------------------------------------------------------
The BC [British Columbia] Centre for Disease Control (BCCDC) Virology
Laboratory routinely sequences the hemagglutinin (HA) gene from a
sample of influenza viruses submitted each season by community
clinicians, hospitals and care facilities across the province of
British Columbia, Canada.

Until mid-February 2009, amino acid sequences of the HA gene of H3
viruses in BC were virtually identical to the vaccine strain [A/
Brisbane/10/07 (H3N2)], with the exception of a Lys189Gln change at
antigenic site B. In early March 2009, however, we detected
additional differences from the vaccine strain among BC viruses
collected from facility outbreak settings at antigenic site B to
include change from the vaccine strain at Asp160Lys (as well as
Lys189Gln) and at antigenic site D at Val229Ala. These changes were
seen only in viruses from care facility outbreaks and not from
community specimens submitted by our network of sentinel physicians.

After the novel North American influenza A/H1N1 virus was reported
from Mexico as well as California during the 4th week of April 2009,
specimens from returning travelers and others in BC with
influenza-like illness were tested including influenza subtype
determination and sequencing. Among approximately 900 respiratory
specimens submitted to the BCCDC laboratory between 24 Apr 2009 and 3
May 2009, the majority was negative for influenza; an equal number of
influenza A detections were of the H1 or H3 subtype.
We have sequenced the HA gene of one of the H3 viruses from an ill
traveler returning from Mexico and find it shares the same amino acid
changes noted above.

These amino acid substitutions do not fulfill the criteria proposed
by Cox as corresponding to meaningful antigenic drift (requiring at
least 2 amino acid substitutions at 2 or more defined antigenic sites
A-E)[1] They may, however, signal important evolution in the HA gene.
During late March and early April 2009 we reported an unexpected
number of late-season care facility outbreaks due to H3 influenza. We
should thus remain vigilant for further H3N2 evolution and reduced
vaccine relatedness since A/Brisbane/10/07(H3N2) has been retained as
the proposed vaccine component for both the 2009 southern and 2009-10
northern hemisphere influenza seasons. Ongoing gene sequence analysis
of H3 viruses from other countries would be informative. In BC, these
H3 mutations arose sometime in early March 2009 and we observe at
least one returning traveler to have likely acquired illness due to
this virus in Mexico (specimen collected in BC 26 Apr 2009). We thus
also wonder to what extent the profile of influenza-like illness
initially reported from mid-March in Mexico may in part be attributed
to this H3N2 variant in addition to emergence of the novel A/H1N1 virus.

Reference:
----------
[1] Cox NJ, Bender CA. The molecular epidemiology of influenza
viruses. S/eminars in /VIROLOGY 1995; 6:359-370.

Authors:
Danuta M Skowronski MD, MHSc, FRCPC, Tracy Chan BSc, Naveed Z Janjua
MD, DrPH, Travis Hottes MSc, Annie Mak BSc, Martin Petric PhD, FCCM,
Mel Krajden MD, FRCPC, Patrick Tang MD, PhD, FRCPC, David Patrick MD,
MHSc, FRCPC, Robert Brunham MD, FRCPC.

At: The BC Centre for Disease Control Provincial Laboratories and
Epidemiology Services

--
Communicated by:
Phil Temples
<phil@temples.com>

[The novel observations reported above reveal the occurrence of
progressive variation in the HA gene of H3N2-type seasonal influenza
virus which if maintained may have consequences for the outcome of
the next seasonal influenza vaccination programme. More intriguing is
the observation that the same novel mutational changes were detected
among viruses isolated from patients in care facilities in Canada as
in a virus isolated from a traveler from Mexico. The authors suggest
that the profile of influenza-like illness initially reported from
mid-March 2009 in Mexico may in part be attributed to this H3N2
variant in addition to the emergence of the novel A/H1N1 virus. This
is a matter that merits urgent investigation as it might help to
explain some of the unusual features of the current epidemic. - Mod.CP]
 
Re: What's on the genetic menu for New A/H1N1 and seasonal A/H1N1 & A/H3N2 swapping?

PB1-F2 is in most of the similar viruses
it had been responsible for 1918 virulence
PB1 was exchanged in 1957 and 1968

suppose this virus gets PB1 from seasonal flu - they should test it
(and tell us the result)
 
Re: What's on the genetic menu for New A/H1N1 and seasonal A/H1N1 & A/H3N2 swapping?

gsgs said:
PB1-F2 is in most of the similar viruses
it had been responsible for 1918 virulence
PB1 was exchanged in 1957 and 1968

suppose this virus gets PB1 from seasonal flu - they should test it
(and tell us the result)
Click to expand...

Could clarify "similar" and "exchanged" please?

To take your statements in reverse sequence ... PB1 is in seasonal flu, it is responsible for 1918 virulence , & it is in "similar" viruses - implies seasonal and "similar" viruses should have a 1918 virulence (but they don't). Maybe you could restate the logic there. All these details are terribly confusing for many people.

A link to a scientific paper for PB1-F2 A/1918 would be nice for newcomers.

Thanks.

.
 
Re: What's on the genetic menu for New A/H1N1 and seasonal A/H1N1 & A/H3N2 swapping?

I already posted the link (N66S in PB1-F2 responsible for 1918-virulence
or such, Palese et.al AFAIR)

exchanged = reassorted
1957 : new Avian HA,NA,PB1
1968 : new Avian HA,PB1

similar = American H1N1 in swine since 1998



http://www.flutrackers.com/forum/showthread.php?t=37360


seasonal flu is not so virulent, because we are adapted,partly immune to it.
Also there are other markers for virulence , we don't know how they "cooperate"
 
Re: What's on the genetic menu for New A/H1N1 and seasonal A/H1N1 & A/H3N2 swapping?

In Italy several antigenic variations has been observed in H3N2 strain, as reported previuosly (I ask someone to verify the substitutions in relation to above ProMed description):

Italia. SORVEGLIANZA VIROLOGICA DELL?INFLUENZA (a cura del Ministero della Sanit? / ISS - 5 febbraio 2009)

SORVEGLIANZA VIROLOGICA DELL?INFLUENZA

4 Febbraio 2009

Aggiornamento settimana 5/09

[Documento PDF originale presso il sito del Ministero della Salute. EDITATO.]


-- ITALIA

Continua la raccolta dei campioni clinici presso i Laboratori periferici della rete Influnet.

Durante questa settimana di sorveglianza sono stati raccolti 163 campioni, di cui 21 positivi al virus influenzale.

In particolare, sono stati identificati e/o isolati 19 virus di tipo A di cui 12 H3. Sono stati, inoltre, identificati 2 virus di tipo B.

Vengono segnalati, dal laboratorio dell?Universit? di Genova, 8 campioni positivi per Virus Respiratorio Sinciziale (RSV).

Nella tabella e nel grafico, di seguito riportati, vengono riassunti i dati virologici complessivi, ottenuti dall?inizio della stagione influenzale (sett. 46-08) ad oggi (sett. 5-09).

[ SETTIMANA 46 - 47 - 48 - 49 - 50 - 51 - 52 - 1 - 2 - 3 - 4 - 5 - TOTALE ]

-- FLU A - 3 - 4 - 4 - 8 - 7 - 11 - 17 - 35 - 47 - 84 - 60 - 19 - 299
-- A (non sottotipizzato) - ... - ... - ... - ... - ... - 2 - 2 - 13 - 11 - 9 - 4 - 7 - 48
-- A/H3N2 - 3 - 4 - 4 - 8 - 7 - 9 - 15 - 22 - 36 - 69 - 54 - 12 - 243
-- A/H1N1 - ... - ... - ... - ... - ... - ... - ... - ... - ... - 6 - 2 - ... - 8
-- FLU B - 0 - 0 - 2 - 0 - 1 - 1 - 0 - 1 - 0 - 0 - 2 - 2 - 9

-- TOT CAMPIONI POSITIVI - 3 - 4 - 6 - 8 - 8 - 12 - 17 - 36 - 47 - 84 - 62 - 21 - 308

N.B. Le apparenti discrepanze rispetto alla tabella della settimana scorsa sono dovute agli aggiornamenti conseguenti ad approfondimenti nelle analisi diagnostiche (tipo/sottotipo).

<table style="width: auto;"><tbody><tr><td></td></tr><tr><td style="font-family: arial,sans-serif; font-size: 11px; text-align: right;">From TABLES</td></tr></tbody></table>

<table style="width: auto;"><tbody><tr><td></td></tr><tr><td style="font-family: arial,sans-serif; font-size: 11px; text-align: right;">From TABLES</td></tr></tbody></table>

In Figura 1 vengono riportate le relazioni filogenetiche relative alla porzione HA1 della HA di virus influenzali A/H3N2 isolati in Italia nella presente stagione 2008/09, confrontati con isolati della precedente stagione. Dall?albero, risulta evidente la derivazione di questi ceppi dalla variante vaccinale A/Brisbane/10/2007, con cui condividono 2 cambiamenti aminoacidici (G50E e K140I) rispetto al vecchio ceppo A/Wisconsin/67/2005. Tuttavia, tutti i virus italiani mostrano una recente importante sostituzione (K173Q) nel sito antigenico E, rispetto al ceppo australiano, riscontrata nel ceppo di riferimento pi? recente A/Wisconsin/5/2008.

Figura 1. Relazioni filogenetiche relative al dominio HA1 della HA di recenti isolati umani A/H3N2 in Italia. L?analisi filogenetica ? stata eseguita presso l?ISS, utilizzando il metodo Kimura 2 per il calcolo delle distanze genetiche e l?algoritmo Neighbor-Joining per la costruzione dell?albero filogenetico.


-- NOTIZIE dal MONDO

- EUROPA

La circolazione dei virus influenzali nei paesi europei ? in sostenuto aumento ed i virus A/H3 sono ancora dominanti. In particolare, durante quest?ultima settimana sono stati raccolti un totale di 3779 campioni clinici: di questi 1904 (50%) sono risultati positivi ai virus influenzali.

Tra questi 1824 di tipo A (803 H3, 59 H1 e 962 non sotto tipizzati) e 80 di tipo B.

E? da segnalare che il 97% dei virus di sottotipo A/H1N1 analizzati ? resistente all?Oseltamivir, mentre resta sensibile allo Zanamivir ed agli inibitori della proteina M2; al contrario tutti i virus di sottotipo A/H3N2 testati risultano sensibili sia all?Oseltamivir che allo Zanamivir, seppur resistenti agli inibitori della proteina M2.

Per ulteriori informazioni ? possibile consultare i seguenti siti:
http://www.eiss.org/index.cgi
http://www.grog.org/


-- USA

La circolazione dei virus influenzali ? in aumento. Sono stati raccolti ed analizzati 3711 campioni, di cui 588 (15.8%) positivi. Tra questi, 508 di tipo A (74 H1, 14 H3, 420 non ancora sotto tipizzati). I restanti 80 appartengono al tipo B.

I virus A sono correlati alla variante vaccinale corrente.

Si riporta, inoltre, l?avvenuto passaggio di un virus suino A/H1N1 all?uomo segnalato nella settimana 3.

Per ulteriori informazioni ? possibile consultare il sito:
http://www.cdc.gov/flu/
-
-----
 
Re: What's on the genetic menu for New A/H1N1 and seasonal A/H1N1 & A/H3N2 swapping?

Some of these changes described by Mamabird have to do with transmissibility/replication efficiency and some with virulence. Just to reiterate some of the competing views of influenza evolution....

Under the recombination view of influenza evolution, (not widely accepted), single amino acid changes such as those listed are not 'random mutations' but can be picked up by interacting with other viruses that already contain these changes. This is similar to the widely accepted reassortment mechanism where influenza viruses exchange whole gene segments (ie HA, PB2) but related to smaller subgene segments of exchange even to the point of single nucleic acids.

Under this scheme the closer two viruses are in any single gene the more likely they are to recombine to exchange these small segments of genetic information. So this widely circulating swine flu, (novel H1N1, 2009), brings new cards to the table and its human, swine and avian lineage could make it more compatible to some of the other cirulating viruses....
 
Re: What's on the genetic menu for New A/H1N1 and seasonal A/H1N1 & A/H3N2 swapping?

Based on Mamabirds list above, I found the following. It needs additional info by those of you more expert than myself.

MAMABIRD?S MOST WANTED LIST

PB2
L(F)475M - is in some human H5N1 & increases virulence by enhancing replicative efficiency (http://www.pnas.org/content/106/9/3366.long )
D567N action ?)
E627K - affects replication efficiency. The presence of lysine leads to more aggressive viral replication, overwhelming the host's defense mechanisms and resulting in high mortality rates in mice.


PB1 none (?)

PB1-F2 - appears to enhance virus-induced cell death in a cell type-dependent manner.
P28L (action ?)
D55N (action ?)
I(V)100A (action ?)
T552S - I think it?s involved in the refolding to form the active sites that are needed for the production of capped RNA primers and for the ensuing synthesis of viral mRNA.


HA multi-basic amino acids at the cleavage site (poultry infections);

NP
G16D - distinguishes human A/H1N1 from avian/swine/equine - a ?D? indicates evolutionary stability, & is associated with NP cleavage in non-avians
L283P - distinguishes human A/H1N1 from avian/swine/equine - involved in the induction of different T-cell responses by each host
F313Y - distinguishes human A/H1N1 from avian/swine/equine

MP
I15V (action ?)
K101R - changes can affect virus morphology
A166V (action ?)
N207S (?T-cell epitopes)

M2
E16G (action ?)
S20N (action ?)

NS none;

NS2 none;

NA
H274Y - confers high-level resistance to neuraminidase inhibitors
anti-viral oseltamivir
N294S - confer resistance to neuraminidase inhibitors
anti-viral oseltamivir

.
 
Re: What's on the genetic menu for New A/H1N1 and seasonal A/H1N1 & A/H3N2 swapping?

I need all these in one file, computer-readable
and nucleotide-numbering in v-flu coding region
then I can chack for any changes easily automatically...



M2,31,S,N,A/N1,Adamantane,N5
M2,26,L,F,A/N1,Adamantane,L
M2,27,V,A,A/N1,Adamantane,V
M2,30,A,T,A/N1,Adamantane,A
M2,34,G,E,A/N1,Adamantane,G
NA,275,H,Y,A/N1,Oseltamivir,H5
NA,293,R,K,A/N2*,Oseltamivir,R
NA,295,N,S,A/N2*,Oseltamivir,N
NA,119,E,V,A/N2*,Oseltamivir,E
NA,119,E,G,A/N2*,Zanamivir,E
NA,119,E,A,A/N2*,Zanamivir,E
NA,119,E,N,A/N2*,Zanamivir,E
NA,152,R,K,B*,Oseltamivir,
PB1-F2,66,N,S,Virulence,Protein,
PB2,199,A,S,Transmission*,A,
PB2,627,E,K,Virulence,E,
PB2,661,A,T,Transmission*,A,
PB2,667,V,I,Transmission*,V,
PB2,701,D,N,Virulence,D,
PB2,702,K,R,Transmission*,K,
PA,409,S,N,Transmission*,N,
NP,136,L,M,Transmission*,I,
NA,??,stalk,No,19a.a.,Transmission*,No,
M2,16,A,G,Transmission*,E,
M2,55,C,F,Transmission*,F,
NS1,92,T,E,Virulence**,D,


PB2:
L475M
D567N
E627K

PB1:
P28L
D55N
I100A
T552S

NP:
G16D
L283P
F313Y

M:
I15V
K101R
A166V
N207S

M2:
E16G
S20N

NA:
H274Y
N294S

HA:
Asp160Lys
Lys189Gln
Val229Ala

PB2:
A199S;

PB1
N(T)375S; PB1-F2 P(R)48Q;

PA
T129I
S409N

HA
E190D
S221P
F251L
Y258F

NP V33I
R100V
Q357K

MP K27R
I168T
N224S

NS2
F55L

. PB2 L(F)475M, D567N and E627K; PB1 none; PB1-F2 P28L, D55N, I(V)100A and T552S; HA multi-basic amino acids at the clevage site (usually associated only with poultry infections); NP G16D, L283P and F313Y; MP I15V, K101R, A166V and N207S; M2 E16G and S20N; NS none; NS2 none; NA H274Y and N294S.



avian_position_human markers

PB2:A44S,M64T,A199S,T271A,L475M,D567N,A588I,E627K,A674T,K702R
PA:P28L,D55N,R57Q,V100A,S225C,L268I,A337S,A404S,S409N,T552S
NP:G16D,I61L,L283P,R305K,F313Y,Q357K
M1:V115I,T121A,T137A
NS1:I81M,P215T,E227R

keyword Finkelstein, diary 1600

PB2:Q151H,R324S,Y432H
PB1:G370A,S466F,V646M,F665S
PA:L581M,P702L
HA:I7V,M8L,N215Y,V351A
NP:A29V,K192E,D202N,T222M,I373T,Y375D
NA:G95S,E96G,H100Y,L123S,C334S
M1:R222H
NS1:T104M,I134F
M2:
NS2:E89A

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

keywords: mamabird ,FT 228987

PB2:A199S
PB1:N(T)375S
PB1-F2:P(R)48Q
PA:T129I,S409N
HA:E190D,S221P,F251L,Y258F
NP:V33I,R100V,Q357K
M1:K27R,I168T,N224S
NS2:F55L


PB2:L(F)475M,D567N,E627K
PB1:P28L,D55N,I(V)100A,T552S
NP:G16D,L283P,F313Y
MP:I15V,K101R,A166V,N207S
M2:E16G,S20N
NA:H274Y,N294S



joined list:

PB2:A44S,M64T,Q151H,A199S,T271A,R324S,Y432H,L475M,D567N,A588I,E627K,A674T,K702R
PB1:P28L,D55N,I100A,G370A,N375S,S466F,T552S,V646M,F665S
PB1-F2:P48Q
PA:P28L,D55N,R57Q,V100A,T129I,S225C,L268I,A337S,A404S,S409N,T552S,L581M,P702L
HA:I7V,M8L,E190D,N215Y,S221P,F251L,Y258F,V351A
NP:G16D,A29V,V33I,I61L,R100V,K192E,D202N,T222M,L283P,R305K,F313Y,Q357K,I373T,Y375D
NA:G95S,E96G,H100Y,L123S,H274Y,H275Y,N294S,N295S,C334S
M2:E16G,S20N
M1:I15V,K27R,K101R,V115I,T121A,T137A,A166V,I168T,N207S,R222H,N224S
NS1:I81M,T104M,I134F,P215T,E227R
NS2:F55L,E89A


A1741C(3),C1118T(5)
A0588G(3),A1741C(3),C0022A(4),C1118T(5),A0283G(6),C0738A(8)
G0799A(1),A1741C(3),G0687T(4),A0877G(4),G1173A(4),C1118T(5)
A1577G(1),A1741C(3),C1118T(5)
G1308A(1),T0450C(2),A0561C(3),G1173A(4),G1563A(4),G0522A(7),A0775G(8)
A1218G(1),G1986T(3),A1044G(6)
G0546A(1)
G0546A(1),A2030G(1),A0300G(2),A1058G(2),A0008G(3),C0145A(4),C0132T(5)
G0298A(5),G1143A(5),G0316A(6)
T1711C(1),G1945A(1),G0636A(2),T2000C(2),G0936A(3),G0298A(5),G1143A(5),G0316A(6),G0456A(8)
C1408T(4),G0298A(5),G1143A(5),G0316A(6),A0742G(6)
G2163A(1),T0658A(4),C1408T(4),G0298A(5),G1143A(5),G1248A(5),G0316A(6),A0742G(6),G0492A(7),G0600A(7),A0367G(8)


--------------sorting...------------------

these 113:

Code: 
PB2,A44S
PB2,M64T
PB2,Q151H
PB2,A199S
PB2,T271A
PB2,R324S
PB2,Y432H
PB2,L475M
PB2,D567N
PB2,A588I
PB2,E627K
PB2,A661T
PB2,V667I
PB2,A674T
PB2,D701N
PB2,K702R

PB1,P28L
PB1,D55N
PB1,I100A
PB1,G370A
PB1,N375S
PB1,S466F
PB1,T552S
PB1,V646M
PB1,F665S
PB1-F2,P28L
PB1-F2,P48Q
PB1-F2,D55N
PB1-F2,N66S
PB1-F2,I100A
PB1-F2,T552S

PA,P28L
PA,D55N
PA,R57Q
PA,V100A
PA,T129I
PA,S225C
PA,L268I
PA,A337S
PA,A404S
PA,S409N
PA,T552S
PA,L581M
PA,P702L

HA,I7V
HA,M8L
HA,D160K
HA,K189Q
HA,E190D
HA,N215Y
HA,S221P
HA,V229A
HA,F251L
HA,Y258F
HA,V351A

NP,G16D
NP,A29V
NP,V33I
NP,I61L
NP,R100V
NP,L136M
NP,K192E
NP,D202N
NP,T222M
NP,L283P
NP,R305K
NP,F313Y
NP,Q357K
NP,I373T
NP,Y375D

NA,G95S
NA,E96G
NA,H100Y
NA,E119A
NA,E119G
NA,E119N
NA,E119V
NA,L123S
NA,R152K
NA,H274Y
NA,H275Y
NA,R293K
NA,N294S
NA,N295S
NA,C334S

M2,A16G
M2,E16G
M2,S20N
M2,L26F
M2,V27A
M2,A30T
M2,S31N
M2,G34E
M2,C55F

M1,I15V
M1,K27R
M1,K101R
M1,V115I
M1,T121A
M1,T137A
M1,A166V
M1,I168T
M1,N207S
M1,R222H
M1,N224S

NS2,F55L
NS1,I81M
NS2,E89A
NS1,T92E
NS1,T104M
NS1,I134F
NS1,P215T
NS1,E227R

proteins enumeration

Code: 
>A/Mexflu/index/2009-02-01
PB2,759,MERIKELRDLMSQSRTREILTKTTVDHMAIIKKYTSGRQEKNPALRMKWMMAMRYPITADKRIMDMIPERNEQGQTLWSKTNDAGSDRVMVSPLAVTWWNRNGPTTSTVHYPKVYKTYFEKVERLKHGTFGPVHFRNQVKIRRRVDTNPGHADLSAKEAQDVIMEVVFPNEVGARILTSESQLAITKEKKEELQDCKIAPLMVAYMLERELVRKTRFLPVAGGTGSVYIEVLHLTQGTCWEQMYTPGGEVRNDDVDQSLIIAARNIVRRAAVSADPLASLLEMCHSTQIGGVRMVDILRQNPTEEQAVDICKAAIGLRISSSFSFGGFTFKRTSGSSVKKEEEVLTGNLQTLKIRVHEGYEEFTMVGRRATAILRKATRRLIQLIVSGRDEQSIAEAIIVAMVFSQEDCMIKAVRGDLNFVNRANQRLNPMHQLLRHFQKDAKVLFQNWGIESIDNVMGMIGILPDMTPSTEMSLRGIRVSKMGVDEYSSTERVVVSIDRFLRVRDQRGNVLLSPEEVSETQGTEKLTITYSSSMMWEINGPESVLVNTYQWIIRNWEIVKIQWSQDPTMLYNKMEFEPFQSLVPKATRSRYSGFVRTLFQQMRDVLGTFDTVQIIKLLPFAAAPPEQSRMQFSSLTVNVRGSGLRILVRGNSPVFNYNKATKRLTVLGKDAGALTEDPDEGTSGVESAVLRGFLILGKEDKRYGPALSINELSNLAKGEKANVLIGQGDVVLVMKRKRDSSILTDSQTATKRIRMAIN}
PB1,757,MDVNPTLLFLKIPAQNAISTTFPYTGDPPYSHGTGTGYTMDTVNRTHQYSEKGKWTTNTETGAPQLNPIDGPLPEDNEPSGYAQTDCVLEAMAFLEESHPGIFENSCLETMEVVQQTRVDKLTQGRQTYDWTLNRNQPAATALANTIEVFRSNGLTANESGRLIDFLKDVMESMNKEEIEITTHFQRKRRVRDNMTKKMVTQRTIGKKKQRLNKRGYLIRALTLNTMTKDAERGKLKRRAIATPGMQIRGFVYFVETLARSICEKLEQSGLPVGGNEKKAKLANVVRKMMTNSQDTEISFTITGDNTKWNENQNPRMFLAMITYITRNQPEWFRNILSMAPIMFSNKMARLGKGYMFESKRMKIRTQIPAEMLASIDLKYFNESTKKKIEKIRPLLIDGTASLSPGMMMGMFNMLSTVLGVSILNLGQKKYTKTIYWWDGLQSSDDFALIVNAPNHEGIQAGVDRFYRTCKLVGINMSKKKSYINKTGTFEFTSFFYRYGFVANFSMELPSFGVSGVNESADMSIGVTVIKNNMINNDLGPATAQMALQLFIKDYRYTYRCHRGDTQIQTRRSFELKKLWDQTQSKVGLLVSDGGPNLYNIRNLHIPEVCLKWELMDDDYRGRLCNPLNPFVSHKEIDSVNNAVVMPAHGPAKSMEYDAVATTHSWIPKRNRSILNTSQRGILEDEQMYQKCCNLFEKFFPSSSYRRPVGISSMVEAMVSRARIDARVDFESGRIKKEEFSEIMKICSTIEELRRQK}
PA ,716,MEDFVRQCFNPMIVELAEKAMKEYGEDPKIETNKFAAICTHLEVCFMYSDFHFIDERGESIIVESGDPNALLKHRFEIIEGRDRIMAWTVVNSICNTTGVEKPKFLPDLYDYKENRFIEIGVTRREVHIYYLEKANKIKSEKTHIHIFSFTGEEMATKADYTLDEESRARIKTRLFTIRQEMASRSLWDSFRQSERGEETIEEKFEITGTMRKLADQSLPPNFSSLENFRAYVDGFEPNGCIEGKLSQMSKEVNAKIEPFLRTTPRPLRLPDGPLCHQRSKFLLMDALKLSIEDPSHEGEGIPLYDAIKCMKTFFGWKEPNIVKPHEKGINPNYLMAWKQVLAELQDIENEEKIPRTKNMKRTSQLKWALGENMAPEKVDFDDCKDVGDLKQYDSDEPEPRSLASWVQNEFNKACELTDSSWIELDEIGEDVAPIEHIASMRRNYFTAEVSHCRATEYIMKGVYINTALLNASCAAMDDFQLIPMISKCRTKEGRRKTNLYGFIIKGRSHLRNDTDVVNFVSMEFSLTDPRLEPHKWEKYCVLEIGDMLLRTAIGQVSRPMFLYVRTNGTSKIKMKWGMEMRRCLLQSLQQIESMIEAESSVKEKDMTKEFFENKSETWPIGESPRGVEEGSIGKVCRTLLAKSVFNSLYASPQLEGFSAESRKLLLIVQALRDNLEPGTFDLGGLYEAIEECLINDPWVLLNASWFNSFLTHALK}
HA ,566,MKAILVVLLYTFATANADTLCIGYHANNSTDTVDTVLEKNVTVTHSVNLLEDKHNGKLCKLRGVAPLHLGKCNIAGWILGNPECESLSTASSWSYIVETSSSDNGTCYPGDFIDYEELREQLSSVSSFERFEIFPKTSSWPNHDSNKGVTAACPHAGAKSFYKNLIWLVKKGNSYPKLSKSYINDKGKEVLVLWGIHHPSTSADQQSLYQNADAYVFVGSSRYSKKFKPEIAIRPKVRDQEGRMNYYWTLVEPGDKITFEATGNLVVPRYAFAMERNAGSGIIISDTPVHDCNTTCQTPKGAINTSLPFQNIHPITIGKCPKYVKSTKLRLATGLRNVPSIQSRGLFGAIAGFIEGGWTGMVDGWYGYHHQNEQGSGYAADLKSTQNAIDEITNKVNSVIEKMNTQFTAVGKEFNHLEKRIENLNKKVDDGFLDIWTYNAELLVLLENERTLDYHDSNVKNLYEKVRSQLKNNAKEIGNGCFEFYHKCDNTCMESVKNGTYDYPKYSEEAKLNREEIDGVKLESTRIYQILAIYSTVASSLVLVVSLGAISFWMCSNGSLQCRICI}
NP ,498,MASQGTKRSYEQMETGGERQDATEIRASVGRMIGGIGRFYIQMCTELKLSDYDGRLIQNSITIERMVLSAFDERRNKYLEEHPSAGKDPKKTGGPIYRRVDGKWMRELILYDKEEIRRVWRQANNGEDATAGLTHIMIWHSNLNDATYQRTRALVRTGMDPRMCSLMQGSTLPRRSGAAGAAVKGVGTIAMELIRMIKRGINDRNFWRGENGRRTRVAYERMCNILKGKFQTAAQRAMMDQVRESRNPGNAEIEDLIFLARSALILRGSVAHKSCLPACVYGLAVASGHDFEREGYSLVGIDPFKLLQNSQVVSLMRPNENPAHKSQLVWMACHSAAFEDLRVSSFIRGKKVIPRGKLSTRGVQIASNENVETMDSNTLELRSRYWAIRTRSGGNTNQQKASAGQISVQPTFSVQRNLPFERATVMAAFSGNNEGRTSDMRTEVIRMMESAKPEDLSFQGRGVFELSDEKATNPIVPSFDMSNEGSYFFGDNAEEYDS}
NA ,469,MNPNQKIITIGSVCMTIGMANLILQIGNIISIWISHSIQLGNQNQIETCNQSVITYENNTWVNQTYVNISNTNFAAGQSVVSVKLAGNSSLCPVSGWAIYSKDNSVRIGSKGDVFVIREPFISCSPLECRTFFLTQGALLNDKHSNGTIKDRSPYRTLMSCPIGEVPSPYNSRFESVAWSASACHDGINWLTIGISGPDNGAVAVLKYNGIITDTIKSWRNNILRTQESECACVNGSCFTVMTDGPSNGQASYKIFRIEKGKIVKSVEMNAPNYHYEECSCYPDSSEITCVCRDNWHGSNRPWVSFNQNLEYQIGYICSGIFGDNPRPNDKTGSCGPVSSNGANGVKGFSFKYGNGVWIGRTKSISSRNGFEMIWDPNGWTGTDNNFSIKQDIVGINEWSGYSGSFVQHPELTGLDCIRPCFWVELIRGRPKENTIWTSGSSISFCGVNSDTVGWSWPDGAELPFTIDK}
PB1-F2,90,MEQEQDTPWTQ}TEHTNTQKRESGRQTQRLVHPSSTRLMDHYLRIMNQVGMHKQTVF}RLWLSLKNPTQEYLRIHALKQWKLFNKQG}IN}
M1 ,252,MSLLTEVETYVLSIIPSGPLKAEIAQRLESVFAGKNTDLEALMEWLKTRPILSPLTKGILGFVFTLTVPSERGLQRRRFVQNALNGNGDPNNMDRAVKLYKKLKREITFHGAKEVSLSYSTGALASCMGLIYNRMGTVTTEAAFGLVCATCEQIADSQHRSHRQMATTTNPLIRHENRMVLASTTAKAMEQMAGSSEQAAEAMEVANQTRQMVHAMRTIGTHPSSSAGLKDDLLENLQAYQKRMGVQMQRFK}
M2 , 97,MSLLTEVET PTRSEWECRCSDSSDPLVIAANIIGILHLILWITDRLFFKCIYRRFKYGLKRGPSTEGVPESMREEYQQEQQSAVDVDDGHFVNIELE}
NS1,219,MDSNTMSSFQVDCFLWHIRKRFADNGLGDAPFLDRLRRDQKSLKGRGNTLGLDIETATLVGKQIVEWILKEESSETLRMTIASVPTSRYLSDMTLEEMSRDWFMLMPRQKIIGPLCVRLDQAIMEKNIVLKANFSVIFNRLETLILLRAFTEEGAIVGEISPLPSLPGHTYEDVKNAVGVLIGGLEWNGNTVRVSENIQRFAWRNCDENGRPSLPPEQK}
NS2,121,MDSNTMSSFQ DILMRMSKMQLGSSSEDLNGMVTRFESLKIYRDSLGETVMRMGDLHYLQSRNEKWREQLGQKFEEIRWLIEEMRHRLKATENSFEQITFMQALQLLLEVEQEIRAFSFQLI}

.....now nucleotides...

delete 0,0,0,0,0,0,94,0,688,0,478 nucleotides from the head to align to the
correct reading frame for PB2,PB1,PA,HA,NP,NA,PB1F2,M1,M2,NS1,NS2
 
Re: What's on the genetic menu for New A/H1N1 and seasonal A/H1N1 & A/H3N2 swapping?

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