Differences twixt H1N1 seasonal and pandemic.

[Auburn Boy]

http://www.eurekalert.org/pub_releas...-osb020110.php

Of swine, birds and men -- pandemic H1N1 flu
Hong Kong SAR, China – Current research suggests that pandemic H1N1 influenza of swine origin has distinct means of transmission from the seasonal flu, yet does not result in the pathogenic severity of avian flu viruses. The related report by Chan et al, "Tropism and Innate Host Responses of the 2009 Pandemic H1N1 Influenza Virus in ex Vivo and in Vitro Cultures of Human Conjunctiva and Respiratory Tract,"
<snip>

Just a teaser, the rest of the article is interesting

One very curious point is that the pandemic strain likes the tissues of the eye, indicating a possible important new vector for entry into humans.

[Kassy]

Not that new.

Seen in H7N7, H5N1 too. I don't know the specifics they found in the conjunctiva here.

It also seems to have a different polymerase solution to seasonal flu.

[Kassy]

New biological route for swine flu to human infections



"Transmission of influenza viruses into the human population requires surmounting biological barriers to cross-species infection," says biochemist Jennifer Doudna, the principal investigator for this research. "We have identified an adaptive mutation in the swine origin H1N1 influenza A virus - a pair of amino acid variants termed the 'SR polymorphism' – that enhance replication, and potentially pathogenesis of the virus in humans."

...

The influenza polymerase consists of three proteins dubbed PB1, PB2 and PA, that work with viral RNA and nucleoprotein to transcribe and replicate the influenza genome in a host cell. Earlier work by Doudna and Mehle with avian influenza had shown that a mutation in the viral protein PB2 - whereby glutamic acid is replaced at a certain position on the amino acid chain with lysine - enables the virus to jump from birds to humans. When glutamic acid is retained in PB2, its presence suppresses the polymerase from performing in human cells.

"That's why we were surprised when we looked at the gene sequences for the current H1N1 polymerase," Mehle says. "The viruses were replicating in people yet they retained the inhibitory glutamic acid in PB2."

In their investigation, Mehle and Doudna found that the 2009 H1N1 virus has acquired the SR polymorphism in its PB2 protein that enhances polymerase activity in human cells. To confirm that the SR polymorphism was a new pathway for the virus to infect humans, they introduced the mutation into the PB2 protein of the avian influenza. As with swine influenza, the polymerase activity and viral replication of the avian virus became enhanced in humans.

"The SR polymorphism mutation in PB2 accomplishes the same goal as the change from glutamic acid to lysine," Mehle explains. "The fact that all of the 2009 H1N1 isolates contain this second mutation supports the notion that it is important for transmission into humans, although we don't yet know the relative importance of the changes in the polymerase versus mutations elsewhere in the virus."

...

Structural analysis of the PB2 627 domain has shown that K627
and E627 variants possess nearly identical structures (27). The
primary difference is that a glutamic acid at position 627 disrupts a large positively charged surface on the domain. We modeled
the structure of WT and mutant forms of the S009 PB2 627
domain to assess the electrostatic surface potential (Fig. 2C).
Increased polymerase activity correlates well with the predicted
restoration of the positively charged surface of the 627 domain
(Fig. 2), raising the possibility that the SR mutation stimulates
polymerase function by partially neutralizing E627


See http://thisbluemarble.com/showthread.php?t=22759

[Kassy]

pandmeic

Shouldn't you fix that?

[flourbug]

we just have to keep sweeping up after AB wherever he goes...

[Kassy]

FB ~ you fixed it? Or AB did that?

[flourbug]

It was me, guilty as charged.

[Auburn Boy]

I'm not gunna say..,

Now the tag is wrong.

[Auburn Boy]

Now the tag is not..,

[Kassy]

Originally Posted by flourbug

It was me, guilty as charged.

No problem...someone had to do it. I was wondering if it was even possible for regular members. I think you can change the thread title as a member as long as you can still edit the 1st post but i wasn't sure so i planned this heinous experiment with AB.

[flourbug]

Oh, did I step in and ruin it?

I think you're right about the member edit times, and I think the forum mods can as well (without time limit). I can do it through Edit in Thread Tools.

Go make another typo thread. I'll sit on my hands this time. lol

[Kassy]

Originally Posted by flourbug

Oh, did I step in and ruin it?

I think you're right about the member edit times, and I think the forum mods can as well (without time limit). I can do it through Edit in Thread Tools.

Go make another typo thread. I'll sit on my hands this time. lol

No it's ok...another one will pop up.

I could've just edited it but i was just teasing AB (and having to do less work at the same time ).

[Kassy]

INFLUENZA PANDEMIC (H1N1) (16): MYOCARDITIS IN CHILDREN

...

Fulminant myocarditis due to viral infection is
an uncommon form of acute myocarditis. Influenza
A virus*associated fulminant myocarditis is
exceedingly rare, with only a few cases reported
in the literature. We report the 1st 4 cases of
acute myocarditis in children associated with the
pandemic H1N1 influenza A virus, all occurring
within a 30- day period. Our tertiary care
hospital serves a geographic region that includes
approximately 800 000 children. During the past 3
years, there was an annual average of 2 cases of
acute myocarditis due to suspected viral
etiology, none of which had evidence of influenza
infection. Within a 30-day period in October
2009, there were 3 cases of acute fulminant
myocarditis and 1 case of acute perimyocarditis
at Rady Children's Hospital*San Diego, all
associated with confirmed H1N1 influenza A
infection. There was serologic,
echocardiographic, and/or histologic evidence of
myocardial involvement in all cases . Three
children had echocardiographic evidence of an
acutely decreased myocardial function. One child
died likely due to acute atrioventricular block,
as suggested by severe lymphocytic infiltration
of the conduction system. Two children required
extracorporeal membrane oxygenation support with
gradual improvement of the ventricular systolic
function over a 1-week period, which is typically
observed in patients with fulminant myocarditis (2).

The prevalence of influenza-associated fulminant
myocarditis is not known because of the lack of
comprehensive screening, with only a handful of
clinical cases and autopsy findings reported in
the literature (5*8). Our documented 4 cases
within a 30-day period, compared with our
previous experience, raise the possibility that
the novel [pandemic] H1N1 influenza A virus is
more commonly associated with a severe form of
myocarditis than previously encountered influenza strains.

Our observations warrant a high index of
suspicion for myocarditis in children with H1N1
influenza A infection. Early detection and
aggressive management are paramount. Timely
intervention with circulatory support may
decrease morbidity and mortality, with the
potential for a favorable cardiac prognosis.

http://www.promedmail.org/pls/otn/f?..._ID:1000,81376