Doorbraak bestrijding Avian Flu?

[Cees Binkhorst]

REPLY TO: D66 at nic.surfnet.nl

Het lokaliseren van de drie genen die het voor het virus mogelijk zouden
maken de epitheel barriere in de toegang naar de longen te nemen, kan
mogelijk zorgen voor een doorbraak in de bestrijding.

De bestaande virussen (inclusief de ´gewone´ verkoudheid) kunnen de
barriere van de keel en luchtbuis niet overbruggen door genetische
verschillen in de epitheelcellen in verschillende delen van de luchtbuis.

De genetische virussleutels (om de cellen binnen te dringen) die passen op
het begin (gewone verkoudheid e.d.) passen niet op de latere delen, of
andersom, evenzo voor de H5N1-variant.

http://www.reuters.com/article/newsOne/idUSTRE4BS56420081229

Researchers unlock secrets of 1918 flu pandemic
Mon Dec 29, 2008 5:44pm EST

WASHINGTON (Reuters) - Researchers have found out what made the 1918 flu
pandemic so deadly -- a group of three genes that lets the virus invade
the lungs and cause pneumonia.

They mixed samples of the 1918 influenza strain with modern seasonal flu
viruses to find the three genes and said their study might help in the
development of new flu drugs.

The discovery, published in Tuesday's issue of the Proceedings of the
National Academy of Sciences, could also point to mutations that might
turn ordinary flu into a dangerous pandemic strain.

Yoshihiro Kawaoka of the University of Wisconsin and colleagues at the
Universities of Kobe and Tokyo in Japan used ferrets, which develop flu in
ways very similar to humans.

Usually flu causes an upper respiratory infection affecting the nose and
throat, as well as so-called systemic illness causing fever, muscle aches
and weakness.

But some people become seriously ill and develop pneumonia. Sometimes
bacteria cause the pneumonia and sometimes flu does it directly.

During pandemics, such as in 1918, a new and more dangerous flu strain
emerges.

"The 1918 influenza pandemic was the most devastating outbreak of
infectious disease in human history, accounting for about 50 million
deaths worldwide," Kawaoka's team wrote.

It killed 2.5 percent of victims, compared to fewer than 1 percent during
most annual flu epidemics. Autopsies showed many of the victims, often
otherwise healthy young adults, died of severe pneumonia.

"We wanted to know why the 1918 flu caused severe pneumonia," Kawaoka said
in a statement.

They painstakingly substituted single genes from the 1918 virus into
modern flu viruses and, one after another, they acted like garden-variety
flu, infecting only the upper respiratory tract.

But a complex of three genes helped to make the virus live and reproduce
deep in the lungs.

The three genes -- called PA, PB1, and PB2 -- along with a 1918 version of
the nucleoprotein or NP gene, made modern seasonal flu kill ferrets in
much the same way as the original 1918 flu, Kawaoka's team found.

Most flu experts agree that a pandemic of influenza will almost certainly
strike again. No one knows when or what strain it will be but one big
suspect now is the H5N1 avian influenza virus.

H5N1 is circulating among poultry in Asia, Europe and parts of Africa. It
rarely affects humans but has killed 247 of the 391 people infected since
2003.

A few mutations would make it into a pandemic strain that could kill
millions globally within a few months.

Four licensed drugs can fight flu but the viruses regularly mutate into
resistant forms -- just as bacteria evolve into forms that evade
antibiotics.

(Reporting by Maggie Fox, editing by Will Dunham and John O'Callaghan)

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