An argument throws heat; a discussion throws light.
One stems from ego and a closed mind whereas the other comes from an open mind.
An argument is an exchange of ignorance whereas a discussion is an exchange of knowledge.
An argument is an expression of temper whereas a discussion is an expression of logic.
An argument tries to prove who is right whereas a discussion tries to prove what is right.

I wish to enter a discussion with you in order to prove what is right but you don’t even want any of it – you appear to prefer dogmatic assertion to scientifc debate. If this blogsite is here to promote lively and healthy scientific discussion then what or who is preventing it because it’s certainly not me?

Like all trH3N2 isolates it has a HUMAN H3 from the 1990′s and has D225G, which is true for all of the trH3N2 isolates, as well as SEASONAL H3N2 circulating in the mid to late 1990′s. The D225G in seasonal H3N2 TRANSMITS (as do recent trH3N2 cases base on sequence similarities.

Discussion of paper at
http://fluboard.rhizalabs.com/forum/viewtopic.php?f=5&t=6297

Precisely how did the Norwegian Institute of Public Health isolate the H1N1 influenza virus from which the alleged ‘mutation’ is supposed to cause a change from aspartic acid to glycine at position 225 of the alleged viral HA protein???? I bet one doesn’t get a really convincing scientific answer to that question, but until this question is effectively answered the physical existence of H1N1 will remain an unproven dogma.

My last comment didn’t make it to the blog – perhaps one struck a nerve somewhere. I thought that science is supposed to be an open book and is about posing and solving specific problems. The question of the effective isolation, biochemical characterization etc, of H1N1 is a problem, and that problem has not been solved to date despite all claims to the contrary. All we seem to obtain are speculative experimental conclusions without the premises and a waste of money.

Clearly, D225G strains are not reacting with the vaccine that has been used to vaccinate tens of millions around the globe. Of course, D225 does react. That sounds like a great way to select for D225G. If Vincent is right, no worries. If niman is right, it'll be Katie-bar-the-door.

Bets, gentlemen?

Clearly, D225G strains are not reacting with the vaccine that has been used to vaccinate tens of millions around the globe. That sounds like a great way to select for D225G. If Vincent is right, no worries. If niman is right, it'll be Katie-bar-the-door.

Bets, gentlemen?

Clearly, D225G strains are not reacting with the vaccine that has been used to vaccinate tens of millions around the globe. Of course, D225 does react. That sounds like a great way to select for D225G. If Vincent is right, no worries. If niman is right, it'll be Katie-bar-the-door.

Bets, gentlemen?

Clearly, D225G strains are not reacting with the vaccine that has been used to vaccinate tens of millions around the globe. That sounds like a great way to select for D225G. If Vincent is right, no worries. If niman is right, it'll be Katie-bar-the-door.

Bets, gentlemen?

I don't think I have ever heard anyone say that a LACK of linkage between cases supports evidence of transmission. That's certainly an 'interesting' stance.

A sample of 4 is statistically insignificant as well.

Hand waving about spontaneopus mutations and coincidences of 4 of 4 fatal cases are simply nonsensical exercises. Knock yourself out, If you think the 4 or 4 fatal cases in Ukraine is a coincidence along with a match of the subclade in Norway with D225G, talk to reporters. They might believe you and continue to distribute the “spontaneous mutation” nonsense to a guilible audience.

it could just have been occasional introductions from travelers without spreading.
We saw that often in Europe in May,June

> The same is true for the detection of the same polymorphism in four of four fatalities
> in western Ukraine, where cases were in the two most hard hit Oblasts and not linked

no proof for that. If it typically happens together with other polymorphisms, which are not present
in D225, that I would consider evidence for your view. Do we see this ?

> Do you think that four of four was a coincidence of SPONTANEOUS “mutations”

yes, ATM I consider that the most likely explanation. It seems to be linked to lung-samples,
but lung-viruses can't easily go into sputum and transmit.

D225G TRANSMITS. The number of nonsynonymous HA changes was ONE (D225G).

Comments (hand waving allowed)?

Another isolate from Kiev, which was wild type at position 225, was California/7-like.

The interest in D225G increased dramatically with the outbreak in Ukraine. Large numbers of previously healthy young adults began showing up at emergency rooms coughing up blood and dying within a few days. Both lungs were destroyed within a couple of days, and the large number of cases produced a significant amount of panic. Initially the infections were called a “mystery disease” but had all of the landmarks of a swine H1N1 infection.

Ukraine request help from WHO, who sent in a team of nine and sent samples off to Mill Hill in London. Most of the samples were from the hard hit regions of western Ukraine where hundreds had died.

I had looked at existing sequences and predicted the large number of hemorrhagic cases were due to a receptor binding domain and focused on position 225 which had already changed to D225E, D225N, and D225G in samples collected worldwide. I predicted the change would be D225G.
The sequences were withheld for 1-2 weeks, but were released at GISAID on Nov 18. Ten HA sequences from 10 individuals were included. One had been collected from an earlier cases in Kiev, while the other nine were from three locations in western Ukraine. Phylogenetic analysis showed that all 9 were from the same sub-clade and four had D225G. The next day more demographic data was added, and it was clear that 4 of the 10 patients had died, and all four had D225G. Three were from lung and one was from throat. The five survivors had the same sub-clade, but were wild type for position 225. The samples in the five survivors were nasopharygeal washes. The four positives were from two Oblasts and none were linked, providing STRONG evidence that D225G transmits.

there are hundreds of HA-spikes, some may have 225D and some 225G,
so such a virus could bind to both types of cells. If that combined HA-production
sheme could be encoded genetically wouldn't that make a major advance in flu-genetics ?

no forum yet, sigh

Is there more data on this statement? It would be great to review it.
Thanks

The ferret model isn't terribly convincing either. An early study on the a Mexican strain of swine flu showed an astoundingly high death rate in ferrets although the same strain in people was relatively mild. Other experiments in ferrets concerning the transmissibility of the virus also seemed to contradict observations on human epidemiology.

Equally, of course, I'm not convinced that the mutation should concern us just from genetic speculation.

As far as I'm concerned the question, as to how concerned we should be, is best answered by observation of human clinical subjects.

Below the table, you write “Different isolates of the 2009 H1N1 influenza virus have D at HA at amino acid 190 and mostly D at amino acid 225. The virus prefers to bind to alpha(2,3) linked sialic acids.” and I think you mean (2,6) here too? If not I'm very confused.