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PostPosted: Wed Mar 03, 2010 6:16 am 
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Location: Pittsburgh, PA USA
Dingo wrote:
Stockholm wrote:
PF11 has made a new comment on vaccine escape

http://pf11.blogspot.com/2010/02/ha-230 ... omain.html


Quote:
2010-02-25
HA 230I Receptor Binding Domain Polymorphism Probable for PF11
Current trending indicates a reportable potential for the M230I polymorphism on the Hemagglutinin of PF11. This Receptor Binding Domain change may enhance Vaccine Escape from the currently selected vaccine target candidate, CA/07 X181.

25% probability of HA 230I in PF11 RBS within 90 days.
33% probability of HA 230I in PF11 RBS within 180 days.
These probabilities will be updated as additional data is made public. Transparency at this stage of the pandemic is essential. Release of sequences and clinical data of a finer detail and higher quantity will allow information-based decisions.

Can anyone explain what all that means and its significance?

M230I is a receptor binding change that was seen in H5N1 in the Gharbya cluster in Egypt and was of note because M230I is in all seasonal influenza (both A and B).

http://www.recombinomics.com/News/05200 ... ation.html

The pandemic strain has M230. Therefore, acquisition of M230I would signal further adaptation to humans.

However, I am not sure about its role in immunological escape, or donor sequences, since seasonal flu is becoming increasingly scarce, therefore I am not sure of the basis for the above probabilities.

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PostPosted: Wed Mar 03, 2010 7:41 am 
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Joined: Sat Jan 30, 2010 2:44 am
Posts: 926
niman wrote:
M230I is a receptor binding change that was seen in H5N1 in the Gharbya cluster in Egypt and was of note because M230I is in all seasonal influenza (both A and B).

http://www.recombinomics.com/News/05200 ... ation.html

The pandemic strain has M230. Therefore, acquisition of M230I would signal further adaptation to humans.

However, I am not sure about its role in immunological escape, or donor sequences, since seasonal flu is becoming increasingly scarce, therefore I am not sure of the basis for the above probabilities.


Thanks. Seems like there's ever increasing mutations of this thing out there.


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PostPosted: Wed Mar 03, 2010 7:46 am 
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Thanks Stephensons for the PM - I tried to reply but it didn't seem to work.


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PostPosted: Wed Mar 03, 2010 8:08 am 
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Location: East of London
Got it Dingo, thanks! :wave:

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PostPosted: Sat Feb 05, 2011 7:34 am 
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Joined: Wed Oct 07, 2009 5:01 am
Posts: 20
Location: USA
niman wrote:
Dingo wrote:
Stockholm wrote:
PF11 has made a new comment on vaccine escape

http://pf11.blogspot.com/2010/02/ha-230i-receptor-binding-domain.html


Quote:
2010-02-25
HA 230I Receptor Binding Domain Polymorphism Probable for PF11
Current trending indicates a reportable potential for the M230I polymorphism on the Hemagglutinin of PF11. This Receptor Binding Domain change may enhance Vaccine Escape from the currently selected vaccine target candidate, CA/07 X181.

25% probability of HA 230I in PF11 RBS within 90 days.
33% probability of HA 230I in PF11 RBS within 180 days.
These probabilities will be updated as additional data is made public. Transparency at this stage of the pandemic is essential. Release of sequences and clinical data of a finer detail and higher quantity will allow information-based decisions.

Can anyone explain what all that means and its significance?

M230I is a receptor binding change that was seen in H5N1 in the Gharbya cluster in Egypt and was of note because M230I is in all seasonal influenza (both A and B).

http://www.recombinomics.com/News/05200802/H5N1_M230I_Migration.html

The pandemic strain has M230. Therefore, acquisition of M230I would signal further adaptation to humans.

However, I am not sure about its role in immunological escape, or donor sequences, since seasonal flu is becoming increasingly scarce, therefore I am not sure of the basis for the above probabilities.



On August 31, 2010, GeneWurx predicted potential for HA 230I in Europe to appear in samples taken by 2010-12-01. Sweden was discussed in a group with Denmark and Norway as having an 85% potential to demonstrate HA 230I within that sample period.

Then the Western world cut sequence publication to a trickle. Only 13 pH1N1 HA sequences since then have come from Sweden. On 2011-02-04, The Swedish Institute for Infectious Disease Control published 3 sequences at GISAID.

One in that subset today, sampled from a 23 year old female on 2010-12-21, carries the HA 230I. Though the sample does post-date our prediction by 20 days, we would suggest that if full publication of the internal databases were to occur, we’d see several 230I sequences as early as October 2010 . . . well within the prediction window.

Withholding data does nothing to invalidate these predictions which have a sample time deadline. Data currency is essential to solving these world health crisis puzzles, but we are willing to wait for corroboration if it takes 50 years to publish 4 month old data.

The 230I sequences are also likely to be circulating in the United States as well, as is evidenced by the ignition markers found in the most recent GISAID US publications of the past two weeks.

This 230I from Sweden, SwedenHalmstad1_23F_2010_12_21, patterns with rare 230I sequences on certain polymorphisms (syn245F, 280A), but then demonstrates extensive homology with the most recent 188T sequences (100N, syn338G, 377K, 454N, 537S), including the fatal UKEngland5040499_2010_12_f.

HA 230I appears to be a jumping polymorphism now and has landed on the most dominant sub-clade in publication (may be biased against actual circulation) around the entire world. The 188T backbone is now demonstrated as permissive to receiving 230I as a tertiary Immune Escape feature.

The SwedenHalmstad1_23F_2010_12_21 sequence falls on a phylogenetic tree branch with one other 188T Swedish sequence from this publication, SwedenVaxjo2_37F_2010_12_22, and 4 contemporary Australian sequences also published this week from Darwin, Sydney and Victoria (2). HA 230I may become popular as a 2011 pH1N1 tertiary Immune Escape feature if these patterns continue.

A 159K change in the HA amino acid range of 156 to 159 (generally associated with Vaccine Escape) is also found on this hybrid virus. The syn245F is also found on a Russian 230I sequence with domaining homology at 158E, 225G, 230I & syn343G. The 280A is found on a 2010 TamiFlu Resistant sequence and may be an HA signal relating to potential for TmX. At any rate, the 280A is conserved in swine with domaining homology at 156E, 225N, 230I & syn346G.

GeneWurx_UK_December_Emerging_Genetics_v5.xls

. . . . SwedenHalmstad1_23F_2010_12_21 (
. . . . . . . . 100N [Slovakia1625_56X_2010_03_30_xL
. . . . . . . . . . . . . . . . . . . . with 230I],
. . . . . . . . 159K [UKEngland4940476_2010_08
. . . . . . . . . . . . . . . . . . . . with 128D, 377K,
. . . . . . . . . . . . . NY3230_2010_01_25
. . . . . . . . . . . . . . . . . . . . with 100N, syn231N],
. . . . . . . . 188T,
. . . . . . . . 230I,
. . . . . . . . syn245F [RussiaBelgorod2_2010_03_15
. . . . . . . . . . . . . . . . . . . . with 158E, 225G, 230I & syn343G],
. . . . . . . . 280A [MXinDRE797_2010_TmX
. . . . . . . . . . . . . swIowa44837_1_2009_11_08_xL
. . . . . . . . . . . . . . . . . . . . with 156E, 225N, 230I & syn346G],
. . . . . . . . syn338G,
. . . . . . . . 377K,
. . . . . . . . 454N,
. . . . . . . . syn537S [UKEngland5040499_2010_12_f])

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PostPosted: Sat Feb 05, 2011 9:14 am 
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Joined: Wed Aug 19, 2009 10:42 am
Posts: 56044
Location: Pittsburgh, PA USA
NS1 wrote:
niman wrote:
[quote="Dingo'][quote]2010-02-25
HA 230I Receptor Binding Domain Polymorphism Probable for PF11
Current trending indicates a reportable potential for the M230I polymorphism on the Hemagglutinin of PF11. This Receptor Binding Domain change may enhance Vaccine Escape from the currently selected vaccine target candidate, CA/07 X181.

25% probability of HA 230I in PF11 RBS within 90 days.
33% probability of HA 230I in PF11 RBS within 180 days.
These probabilities will be updated as additional data is made public. Transparency at this stage of the pandemic is essential. Release of sequences and clinical data of a finer detail and higher quantity will allow information-based decisions.
[/quote]
Can anyone explain what all that means and its significance?[/quote]
M230I is a receptor binding change that was seen in H5N1 in the Gharbya cluster in Egypt and was of note because M230I is in all seasonal influenza (both A and B).

http://www.recombinomics.com/News/05200 ... ation.html

The pandemic strain has M230. Therefore, acquisition of M230I would signal further adaptation to humans.

However, I am not sure about its role in immunological escape, or donor sequences, since seasonal flu is becoming increasingly scarce, therefore I am not sure of the basis for the above probabilities.[/quote]


On August 31, 2010, GeneWurx predicted potential for HA 230I in Europe to appear in samples taken by 2010-12-01. Sweden was discussed in a group with Denmark and Norway as having an 85% potential to demonstrate HA 230I within that sample period.

Then the Western world cut sequence publication to a trickle. Only 13 pH1N1 HA sequences since then have come from Sweden. On 2011-02-04, The Swedish Institute for Infectious Disease Control published 3 sequences at GISAID.

One in that subset today, sampled from a 23 year old female on 2010-12-21, carries the HA 230I. Though the sample does post-date our prediction by 20 days, we would suggest that if full publication of the internal databases were to occur, we’d see several 230I sequences as early as October 2010 . . . well within the prediction window.

[/quote]

I don't think that publication of pH1N1 would fall into the "trickle" category. In general sequences usually have a 3-6 month delay, but sequences from Europe and much of the northern hemisphere has been quite forthcoming. Most sequences from Sweden come from The Swedish Institute for Infectious Disease Control and they have been publixhing recent sequneces from pH1N1, H3N2, and pH1N1 (26 collected since October 1, 2010). They just published three, but they published 8 others in the past few weeks. These sequences have S188T, but also include a sub-clade that does not have S188T or S186P. This subclade was also found at a relative high frequency in Spain and Iraq. Recent sequneces from Denmark were publiched at Genbank and these wequences were dominated by S188T and S186P. The largest number of UK sequences are at GISAID and released by the Health Protection Agency (HPA) or Mill Hill. The HPA initially put out four representative sequences from fatal cases, which was followed by 37 sequences, largely from November and December. These were dominated by S186P and S188T (with S188T in all December sequences). Mill Hill also released a series from the UK (which extended the pattern seen in the HPA sequences). This pattern as also seen in sequences from Luxembourg and Germany. Mill Hill also published sequences from Iran and Egypt, which were similar (and Iran sequneces also came out of Tehran, which also matched). The same was seen in sequences from Bangladesh and India. The CDC also released several series from the US and smaller numbers from Europe and Asia. The WHO regional center in Australia has also rleased recent sequneces from Australia and SE Asia. Russia, Canada, Mongolia, and Thailand have also released recent sequences and all of the above have S188T and S186P in the vast majority of sequences, with S188T dominating in most loications and in the most recent (mid December through January) sequneces.

Thus, the release of sequences, especially those collected since October, 2010 has been quite robust and includes Europe (with sequences from Sweden and Denmark).

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