Rhiza Labs FluTracker Forum

No. E627K is associated with increased virulence in mice and was recently in the news on H3N2/H5N1 reassortants, which involved the acquistion of E627K via human PB2. I would be EXTREMELY surprised if this was not E627K.

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www.twitter.com/hniman

I suspect you have not come across Australian's sense of humour much.

When we see utter crap like SteveMartin's post we do what we call "take the piss" out of them.

Not difficult in his case - in my short time here, I haven't seen one post of his that isn't just a waste of bandwidth.

Dingo, you have not only frightened Dr. Niman.
I thought you had been hit by H1N1v, with a new symptom!

Commentary

http://www.recombinomics.com/News/03161 ... dia_3.html

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www.twitter.com/hniman

It sounds like this Pandemic H1N1 virus, is tweaking itself toward becoming more of a human/swine virus without the feathers and fluff.

I wonder if this could be a reason we're starting to see more positive flu tests at work (after months of flu symptoms with negative results.) Nobody's changed the way we collect samples, the test kits haven't changed, but now a "few" kids who come in with classic flu symptoms are actually testing positive for flu (and here lately their entire families are sick) The sicker patients on ventilators who initially test negative, rarely appear to have close family members who are sick). It's just so unusual to actually get a rapid flu test back, that's positive right off the bat.

If this Pandemic virus widely acquires this change, how close will it be (genetically) to the 1918 virus? Are we moving in that direction? Or away from that direction?

The fact that they "found" it in three samples probably means that it's OUT there significantly.

I'm not looking forward to the next flu season.

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"Old Mother Goose, when she wanted to wander, would ride through the air on a very fine gander."
1916
"Mother Goose had a house,
'Twas built in a wood,
Where an owl at the door
For sentinel stood."

E627K could be generating positive rapid tests because there will be more H1N1 in the upper respiratory tract (which is why H1N1 will be more transmissible and generate higher viral loads).

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www.twitter.com/hniman

Although addition of E627K will match 1918 (as will D225G), the loss of E627K in swine is relatively recent. Not only did the 1918 pandemic strain have E627K, but so did the first swine isolate (H1N1 from 1930) and the first human isolate (H1N1 from 1933). E627K really is mammalian, but triple reassortants which formed in the 1990's replaced swine PB2 with avian, which is why the pandemic strain has avian PB2 with E627.

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www.twitter.com/hniman

but given that the CDC mostly recieves samples from critically ill patients on ventilators (needing confirmation)

and given that an E627K infected patient would most likely test positive on a rapid flu test ~ (Negating any further sample-sending to the CDC)

wouldn't that set the stage for this PB2 change to go undetected for a while in this country? (Unless it's detected in the CDC random sample collecting that they say they do.)

Our whole flu-testing strategy is filled with holes. It's like fishing for viruses with a... "fishnet."

We're gonna need a bigger net. (with WAY smaller holes).

_________________
"Old Mother Goose, when she wanted to wander, would ride through the air on a very fine gander."
1916
"Mother Goose had a house,
'Twas built in a wood,
Where an owl at the door
For sentinel stood."

Niman,

Based purely on reading scientific articles, it seems to me that there was less understanding or agreement amongst the scientific community as to the implications of changes in HA 225. Furthermore, regardless of disagreements in how D225G is acquired (randomly or selectively), the potential effects of D225G seemed to be down played by the WHO.

In contrast it seems that some changes are generally well studied and accepted by the scientific community, such as H274Y conferring oseltamivir resistance. Another changes that I read quite a bit about last year was PB2 627. Last year some articles down played the severity of pH1N1 because it had E627, rather than K627. A published paper last year discussing the role of the SR polymorphism also discussed the effects in human (and swine) of E627K as though the effect of changes in this position are well accepted.

If E627K change keeps showing up, do you think the WHO's response will be more alarming as it seems the scientific community recognizes the significance of this change?

I don't see much of a change in the WHO response. All results are subject to interpretation as well as variation in testing. In UKraine 27/37 fatal lung samples had D225G/N, which is quite striking for a heterogeneous disease like influenza which usually does not kill, but WHO and the CDC still want to discount the result.
H274Y clearly knocks out Tamiflu and Peramivir, but WHO won't say much until it is fixed in pandemic H1N1, as happened to seasonal H1N1.
For E627K, it is more of a when than an if because all human seasonal flu has E627K. WHO can just say that H1N1 in the upper respirtaory tract is better than the lower respiratory tract, so E627K may make H1N1 more transmissible, but milder.

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www.twitter.com/hniman