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Re: Is the mutation in Norway similar to the change in Ukraine?
"G" in 225 is nothing new.
While it was in 2 of the 1918 sequences, the others didn't have it, nor did most of the H1N1 sequences until 1940, when it became the concensus until 1957.
It wasn't present in 1976/HA, despite the many similar values to 1918.
Then starting with 1979, it was once again the predominant value at 225. Slowly, it was "culled from the gene pool" and replaced by a "D", but it still occured with a declining frequency, until there was only about 1 sample per year:
2001 - Egypt
2003 - Georgia (US)
2005 - Thailand (in a very different H1N1)
2007 - Malindi/4837
2008 - Hawaii
early 2009 - St. Louis
To see an abundance of G225 - do an alignment of 1918 to 1957.
One thing that really struck me as I just finished looking at EVERY HA from 1918 thru early 2009, is that in recent years, the virus' HA has really stabilized. It was as if it had tried all its tricks to mutate around the human immune system & had run out of new game plans. It was about time for a totally new game, new players, & new tricks.
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"The next major advancement in the health of American people will be determined by what the individual is willing to do for himself"-- John Knowles, Former President of the Rockefeller Foundation
Re: 225G Preliminary Worldwide Tracking & Evaluation
To see an abundance of G225 - do an alignment of 1918 to 1957.
225 shows up on these alignments at position 239 - the second to the last postion (just prior to the "Q").
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"The next major advancement in the health of American people will be determined by what the individual is willing to do for himself"-- John Knowles, Former President of the Rockefeller Foundation
was it ever during all these years and decades associated
with increased virulence, infection of lungs ?
Cytokene storm in 1918 ?
Don't know without more reading.
However, I just went looking at pig H1N1 in 2008 and 2009.....G225 is in Chinese swine! So whether it was hitchhiking along all this time, OR it recently jumped into the human mix to "join the party" it's hard to say.
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"The next major advancement in the health of American people will be determined by what the individual is willing to do for himself"-- John Knowles, Former President of the Rockefeller Foundation
Re: 225G Preliminary Worldwide Tracking & Evaluation
Of those CHinese swine, the last one has a very different HA - and it has several genes that are the same as the early North American human swine flu.
GenBank: ACU12855.1
hemagglutinin [Influenza A virus (A/swine/Guangdong/2/2009(H1N1))]
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"The next major advancement in the health of American people will be determined by what the individual is willing to do for himself"-- John Knowles, Former President of the Rockefeller Foundation
Re: 225G Preliminary Worldwide Tracking & Evaluation
Ilya [Kolmanovskiy] [Vcher] Ukrainian virus is actually more dangerous than other The analysis of the genetic code of the Ukrainian variety of pig influenza is finished. Alas, in it they found the very unpleasant mutation Already commented 1 + 1 Anatoliy [Volkov] +T- V the beginning of week on the news passed the communication: the Ukrainian variety of influenza H1N1 will analyze international experts - on Yushchenko's request. In popular [bloge] of German biologist (with the Ukrainian roots) it stumbled on the references about the finished results: the experts of WHO (World Health Organization) read the sequences of the code and laid out them into the world data base. It turned out that Ukrainian models contain the mutation D225G, which thus far they did not find in pig influenza - and this all distressed. The chief characteristic of pig influenza, as we more than once wrote, in the fact that it is not limited to the upper respiratory tract, it climbs into the lungs and is caused virus pneumonia (which many doctors treat by antibiotics - which is thoughtless). For this virus it must stick to the surface of the cells of lungs; for this to it is necessary that its protein- feeler (the so-called agglutinins, you hear the here familiar word of glue?) they were well suited the protein- receptors on the surface of cells. With this ability in the pig influenza the matter is very well - in contrast to the seasonal, which remains in the throat. So here, that mutation itself D225G, found in the Ukrainian virus H1N1, this change in the protein- agglutinin, which makes possible for it better to stick to the cells in the lungs how this makes, for example, German virus H1N1. The possibilities of Ukrainian virus in this sense are compared with the sadly known Spaniard. Washings for the analysis are obtained not of the nasopharynx, but directly from the lungs - which additionally confirms ?the place of the registration? of virus. In accordance with this fact, the mortality in the Ukraine is 10 times higher than in Germany: 0,4% against 0,04%, writes the same biologist, [bloger] of pro_genes (here, true, it is not possible to discount difference as medicine). ?Since this influenza is very infectious, continues pro_genes, people rapidly and mass fell ill, and therefore many died simultaneously, which produced psychological impression?. What this does mean? First, the additional argument in favor of vaccine. In the second place, ?if you are gathered to the relatives in the Ukraine - it is worthwhile to endure German virus?, concludes pro_genes. But in the correspondence with me it adds: ?In reality, mass infection by mild cases, alas, increases the probability of further mutations?. As will further mutate and extended influenza H1N1 - it is unknown. On how much will be sufficient the immunity, acquired with the vaccine and the mild cases, it is unknown. We will simply follow the news of science from this region - if the amateurs of oil of krill forgive us. P.S. Not bad lecture of the historian of influenza here. Commentaries 1 + 1 Anatoliy [Volkov] 22:58 yesterday you the site of the doctor of [merkola] attentively read a little or they signed?. I desire further panic with the attempts to damage to its own health? it brings you profession? [OtvetitSsylka] Ilya [Kolmanovskiy] 10:08 today Panic - this, doctor, the lot of your flock - your and doctor [Merkol]. When you and such as you speak: to [uuu], brother, in you everything is neglected: and [karma] of [zasrana], and oil of krill in the blood scarcity. Give- kA I to [pogadayu] on the coffee sediment, that in you not so that to you to prescribe - and not that to you [kranty]. To your audience it is necessary the Messiah, shaman is necessary. And the more he will be strange, the greater the large number of [meynstrimnykh] truths he will place from the feet to the head - the more popular it will be. My audience to panic is immune. The facts, checked by the valuable study, subjected to the independent judgment of associates and competitors, are necessary to it. And these facts to it are necessary in order to think, and to think as them to [proevrit] - and not to take to the faith.
Re: 225G Preliminary Worldwide Tracking & Evaluation
The above makes me wonder if the declining influenza deaths in the last 80 years were due less to antibiotics than they were due to genetic changes (G225N).
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"The next major advancement in the health of American people will be determined by what the individual is willing to do for himself"-- John Knowles, Former President of the Rockefeller Foundation
“… viruses with a similar mutation had been detected in several other countries, including Brazil, China, Japan, Mexico, Ukraine and the United States. "No links between the small number of patients infected with the mutated virus have been found and the mutation does not appear to spread," ...”
If the official statement in today’s Washington Post is accurate concerning the circulating geography of the Norway polymorphism associated with several fatalities, then the only probable selection is 225G. Evaluating the meta-data of available published and partially public sequences, no other SNP of interest corresponds to the range stipulated.
The positive statement indicating low transmissibility of 225G, however, is not supportable at this time by solid evidence due to lack of surveillance using the proper tools and testing protocols. The statement is perhaps intended to assuage rather than inform.
Singapore (4 with 225X encoded from aNy nucleotide) *
While 225G is probable or confirmed with very limited depth in 12 countries, our team is more concerned about the extensive range of 225E at the moment, documented with considerable penetration in at least 21 countries, including island nations and prominent international tourism hotspots. At any measure, the 225Ecirculating range is wider and deeper than 225G though the two overlap geography in at least 6 countries. Linked SNPs of interest appear to be more involved, as 225E demonstrates several clear acquisition paths that are not apparent with 225G.
Though the clinical attributions are not presently noted as a corollary to fatal cases like 225G, the accompanying changes and multiple backgrounds onto which the Glutamate at 225 (225E) is found may eventually provide a substantially more capable viral strain and most certainly is providing co-circulating sub-species of high interest alongside the 225G.
225G does, of course, merit scrutiny due to patterning with 230I on H1N1 Seasonal 2008 and 2009 sequences. If the range of 225G continues to smoulder, an attractant effect may draw 230I due to co-infection in areas that continue to have Seasonal H1N1 strains in circulation. The very high level of bird involvement in transporting genetics across serotypes may provide proximity, attraction and opportunity for H5N1 as a donor candidate for 230I due to verified H5N1 ranges at geographic inflection points for PF11. The world may not yet be seeing this permutation (225G & 230I) because the shortened infection to expiration timing also provides less time for viral recombination.
This 1918 and Avian SNP travels with H1N1 and H5N1 Avian polymorphisms indicating potential wild bird transport vectors. In a human host, the Avian modifications may find advantage at certain tissue types due to body core proximity providing basal temperature increases and may drive replication behaviour. The human lung may be precisely the correct temperature to promote rapid replication, more efficient binding or improved cleavage capability.
Influenza Flux will eventually find the appropriate or optimal combination of genetics to achieve stasis, but until that stasis of PF11<sub>>Ω </sub>is achieved, these sub-species will continue to be quite dangerous, demonstrating varying levels of Cytokinic Dysregulation according the host-pathogen interplay and the viral strain's capacity for temporarily suspending early catalysts to the innate immune response.
As the data are released, including the sequences, presentation and progression, testing protocols, sampling protocols, prognoses, sequencing lab procedures and epidemiology, a higher level of interpretation may be made concerning these polymorphisms based on facts, rather than speculation.
A present 225G sequence set of less than 25 instances within ΣPF11 and those few having little to no associated clinicals does not provide a stable foundation at this time for determination of emergent characteristics such as rate of transmissibility, probability of co-infection with wildtype or spontaneous revision from wt due to tropism upon attaining deep lung infection.
?? viruses with a similar mutation had been detected in several other countries, including Brazil, China, Japan, Mexico, Ukraine and the United States. "No links between the small number of patients infected with the mutated virus have been found and the mutation does not appear to spread," ...?
If the official statement in today?s Washington Post is accurate concerning the circulating geography of the Norway polymorphism associated with several fatalities, then the only probable selection is 225G. Evaluating the meta-data of available published and partially public sequences, no other SNP of interest corresponds to the range stipulated.
The positive statement indicating low transmissibility of 225G, however, is not supportable at this time by solid evidence due to lack of surveillance using the proper tools and testing protocols. The statement is perhaps intended to assuage rather than inform.
Singapore (4 with 225X encoded from aNy nucleotide) *
While 225G is probable or confirmed with very limited depth in 12 countries, our team is more concerned about the extensive range of 225E at the moment, documented with considerable penetration in at least 21 countries, including island nations and prominent international tourism hotspots. At any measure, the 225Ecirculating range is wider and deeper than 225G though the two overlap geography in at least 6 countries. Linked SNPs of interest appear to be more involved, as 225E demonstrates several clear acquisition paths that are not apparent with 225G.
Though the clinical attributions are not presently noted as a corollary to fatal cases like 225G, the accompanying changes and multiple backgrounds onto which the Glutamate at 225 (225E) is found may eventually provide a substantially more capable viral strain and most certainly is providing co-circulating sub-species of high interest alongside the 225G.
225G does, of course, merit scrutiny due to patterning with 230I on H1N1 Seasonal 2008 and 2009 sequences. If the range of 225G continues to smoulder, an attractant effect may draw 230I due to co-infection in areas that continue to have Seasonal H1N1 strains in circulation. The very high level of bird involvement in transporting genetics across serotypes may provide proximity, attraction and opportunity for H5N1 as a donor candidate for 230I due to verified H5N1 ranges at geographic inflection points for PF11. The world may not yet be seeing this permutation (225G & 230I) because the shortened infection to expiration timing also provides less time for viral recombination.
This 1918 and Avian SNP travels with H1N1 and H5N1 Avian polymorphisms indicating potential wild bird transport vectors. In a human host, the Avian modifications may find advantage at certain tissue types due to body core proximity providing basal temperature increases and may drive replication behaviour. The human lung may be precisely the correct temperature to promote rapid replication, more efficient binding or improved cleavage capability.
Influenza Flux will eventually find the appropriate or optimal combination of genetics to achieve stasis, but until that stasis of PF11<sub>>Ω </sub>is achieved, these sub-species will continue to be quite dangerous, demonstrating varying levels of Cytokinic Dysregulation according the host-pathogen interplay and the viral strain's capacity for temporarily suspending early catalysts to the innate immune response, including suppression of RIG-I ubiquination as the viral NS1 protein binds TRIM25 ultimately leading to reduced intra-cellular synthesis of Type I IFN. The timing and the level of RIG-I ubiquination suppression, thus interferon synthesis blocking, may eventually be found as the primary effector of host pathology from this IDRREAV, PF11. We feel that the evidence is well structured toward timing as an effector equal in importance to the level of inactivation / suppression.
225G gets the virus situated in the lung tissue and NS1 blocks the innate response. Add back the rapid replication at a multiplier over the speed of a Seasonal Influenza strain and you find an overwhelming viral load before any cell has signalled for assistance. When millions of viral particles erupt in a concentrated area from the lysed cells, the detritus alone drives an surging cascade of inflammatory cytokines. A slow response creates deadly risk. Then the body must take into account the travelling circus of sub-species that waste no time returning to their hard work of re-engineering the next cell for a viral production line.
As the data on 225G cases are released, including the sequences, presentation and progression, testing protocols, sampling protocols, prognoses, sequencing lab procedures and epidemiology, a higher level of interpretation may be made concerning these polymorphisms based on facts, rather than speculation.
A present 225G sequence set of less than 25 instances within ΣPF11 and those few having little to no associated clinicals does not provide a stable foundation at this time for determination of emergent characteristics such as rate of transmissibility, probability of co-infection with wildtype or spontaneous revision from wt due to tropism upon attaining deep lung infection.
Re: 225G Preliminary Worldwide Tracking & Evaluation
R means: mixed A and G. This is rare, so it's remarkable that we have it here at position
716 which corresponds to D225G.
N means: could be all 4 nucleotides A,C,G,T . Could not be determined (or is mixed ?)
Re: 225G Preliminary Worldwide Tracking & Evaluation
48m, 2nd in Nebraska, April 2009 - was that a severe case ?
what means : passage history E2,C1
passed twice in eggs and then there was the R ?
A/Nebraska/02/2009(H1N1)
VERSION GQ221801.1 GI:238627881
AUTHORS Shu,B., Balish,A., Garten,R., Smith,C., Emery,S., Barnes,J.,
Deyde,V., Klimov,A. and Cox,N.
TITLE Human infection with novel swine H1N1 influenza
JOURNAL Unpublished
AUTHORS Shu,B., Balish,A., Garten,R., Smith,C., Emery,S., Barnes,J.,
Deyde,V., Klimov,A. and Cox,N.
TITLE Direct Submission
JOURNAL Submitted (29-MAY-2009) WHO Collaborating Center for Surveillance,
Epidemiology and Control of Influenza, Influenza Division, Centers
for Disease Control and Prevention, 1600 Clifton Road, N.E.,
Atlanta, GA 30333, USA
submitted 29.May 2009
Host_gender M
Host_age 48
Collection_month 4
Passage_history E2
"R" at 716
A/Nebraska/02/2009(H1N1))
VERSION GQ377082.1 GI:253828574
AUTHORS Shu,B., Balish,A., Garten,R., Smith,C., Emery,S., Barnes,J.,
Deyde,V., Klimov,A. and Cox,N.
TITLE Human infection with novel swine H1N1 influenza
JOURNAL Unpublished
REFERENCE 2 (bases 1 to 1701)
AUTHORS Shu,B., Balish,A., Garten,R., Smith,C., Emery,S., Barnes,J.,
Deyde,V., Klimov,A. and Cox,N.
TITLE Direct Submission
JOURNAL Submitted (14-JUL-2009) WHO Collaborating Center for Surveillance,
Epidemiology and Control of Influenza, Influenza Division, Centers
for Disease Control and Prevention, 1600 Clifton Road, N.E.,
Atlanta, GA 30333, USA
Submitted (14-JUL-2009)
Passage_history C1
"A" at 716
Comment