Deadly 'flu code cracked TheStar.com - News - Deadly 'flu code cracked
January 17, 2007
Joe Hall
Toronto Star
http://www.thestar.com/printArticle/172085
Canadian scientists have helped unlock a key secret to history's deadliest
influenza outbreak and how it killed so quickly and efficiently.
The savage Spanish Flu pandemic that swept the globe at the end of the First
World War killed about 50 million people - many in a matter of hours - when
their immune systems began attacking their own lungs, a paper published today
in the journal Nature says.
The paper, which studied monkeys infected with a reconstructed version of the
1918 flu at Canada's National Microbiology Laboratory in Winnipeg, may also
offer clues on how to stem future outbreaks.
"This research provides an important piece in the puzzle of the 1918 virus,
helping us to better understand influenza viruses and their potential to cause
pandemics," said Darwyn Kobasa, a research scientist with the Public Health
Agency of Canada in Winnipeg and the lead study author.
"Thanks to recent technological advancement, we are able to study this virus
and how it wreaked havoc around the globe," Kobasa said in a statement.
In the early 1990s, University of Toronto geographer Kirsty Duncan, then at
the University of Windsor, located seven young coal miners who had died in 1918
and were buried in a permafrost cemetery in the village of Longyearbyen, Norway
Duncan was able to isolate bits of viral RNA from the miner's preserved
flesh, which has been used to construct copies of the original 1918 virus.
But scientists at the "Level 4" Winnipeg lab - which can house and study the
earth's most lethal pathogens - used viral RNA from archived tissues of first
war soldiers to resurrect the 1918 pathogen, Kobasa said in an interview.
They then used that virus to infect several macaque monkeys and study its
effects on the primates.
What they found was that the virus unleashed an attack of the body's immune
system on the lungs - causing fluids to build up in the respiratory tract.
The flu's victims, the study says, would essentially have drowned in their
own fluids.
"This study in macaques . . . suggests that the host immune response is out
of control in animals infected with the virus," Michael Katze, a microbiologist
at Seattle's University of Washington said in a release on the study.
"Our analysis revealed potential mechanisms of virulence, which we hope will
help us develop novel antiviral strategies to both outwit the virus and
moderate the (human) immune response," said Katze, one of the study's authors.
The same immune response identified in the Winnipeg monkeys has also been
seen in people infected with the H5N1 virus - or avian flu - that is present
today in Asia and has killed 150 people.
"What we see with the 1918 virus in infected monkeys is also what we see with
H5N1," says Yoshihiro Kawaoka, a University of Wisconsin-Madison virologist who
also participated in the study.
Unlike the 1918 Flu, the avian flu has so far been unable to spread easily
between humans.
But Kawaoka suggests that the overwhelming immune response seen in both
varieties may be a signature of all virulent influenza viruses.
Dr Donald Low, chief microbiologist at Toronto's Mount Sinai hospital said
the study helps confirm a theory that has been proposed for some time about the
Spanish flu's rapid and deadly progress.
Low said the study contained strong evidence to the back up the so-called
"cytokine storm" theory of pandemic flu outbreaks.
"There's some pretty nice evidence (in the paper) to show exactly what is
happening," Low says.
Although it "doesn't put it's finger on the exact cause", Low said the paper
strongly suggests that a protein produced by pandemic viruses, known as NS1, is
"essentially hijacking the immune system."
Low said the protein inhibits the immune system's ability to kill off the
invading virus, causing the cytokine messengers that trigger the body's
inflammatory response to flues to keep on going.
Cytokines are chemical messengers in the body that trigger - among other
things -- appropriate responses to invasive agents. And the cytokines involved
in reacting to influenzas typically promote an inflammatory response in the
lungs and other infected organs, Low said.
With the NS1 protein preventing the influenza virus from being killed off,
however, Low said the cytokines triggering lung inflammation just keep on
acting until they eventually destroy the pulmonary lining.
Low said the study also looked at monkeys infected with normal human
influenza and that their cytokine response waned after several days as the
virus was irradiated in the body.
"But if you look at the monkeys with the 1918 strain, it's gone to hell in a
hand cart, you've got bleeding in the lung, you've got fluid in the lung
there's no evidence of any repair."
Low said the study suggests that the virus' protective NS1 protein might be a
prime target for any therapies to protect people against future pandemic flues.
"If we find that what's predictive of real bad disease is this protein that
being produced by the virulent strain . . . in theory there could be a drug
which could actually neutralize NS1."
In all, seven monkeys were infected with the 1918 flu at the Winnipeg lab,
and all developed symptoms within 24 hours. All were so sick after eight days
that they had to be put down for humane reasons.
This type of timetable reflects many reports of the flu's behaviour in the
1918 outbreak.
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