EMBARGOED FOR RELEASE AUG. 17, 5 P.M. EASTERN TIME
CONTACT: Yoshihiro Kawaoka, (608) 265-4925; [email protected]
New Evidence Shows How Some Flu Viruses Become Lethal
MADISON - Studying a descendant of the 1918 influenza virus that killed at
least 20 million people worldwide, University of Wisconsin-Madison virologists
discovered a new molecular trick some viruses use to transform from dangerous
to deadly.
In research detailed in the Aug. 18 Proceedings of the National Academy of
Sciences, UW-Madison virologists Hideo Goto and Yoshihiro Kawaoka have
found a molecular mechanism that allows influenza viruses to cause sweeping
damagethroughout the body. Influenza infection is normally limited to respiratory
systems, but this previously undetected process gives the virus the deadly
ability to attack many organs in the body.
"This finding provides an additional marker for scientists to be aware of in
their surveys of emerging viruses," said Kawaoka. "This could be another
important indicator of whether a virus is dangerous and potentially lethal."
Kawaoka said the extreme virulence of the 1918 influenza virus is a public
health mystery. One of the worst infectious disease outbreaks in human history,
the 1918 flu killed not only vulnerable populations such as the elderly and
young children, but an unusually high number of otherwise healthy young adults.
While this finding offers no definitive explanation for the 1918 virus,
Kawaoka said it is a question that warrants further scientific study.
Kawaoka and Goto, researchers in the UW-Madison School of Veterinary
Medicine, studied a virus closely related to the 1918 strain which appeared
nearly a decade later in humans. The virus is widely studied for its ability to
replicate in the brains of mice, but Kawaoka also found it could replicate in a
number of different organs.
Their discovery concerns proteins on the virus' surface that allow the virus
to attach to target cells. Normally, a viral surface protein called
hemagglutinin must be chopped into two parts before the virus can infect a cell.
The virus uses an enzyme from the cell it is invading to clip the protein.
The enzyme that acts as a "scissors" is normally localized in respiratory
organs, which confines the virus to that part of the body. But in this strain of
virus, Goto and Kawaoka found a unique mechanism at work that could lead to more widespread infection.
A different surface protein on the virus, called neuraminidase, binds and
traps a common enzyme precursor called plasminogen, and this union created a
molecular key that gave the virus access to cells throughout the body, rather
than only the respiratory system.
"The importance of this finding is that it's the first example of a virus using a
binding protein to its benefit when infecting a host," he said. "Our finding may
have much broader implications in the virology field, and will prompt researchers
to look for a protein of this kind in other viruses."
Influenza viruses are never the same threat each year. Their surface
proteins normally undergo slight changes, called "drift," which requires new
vaccines to be developed to protect against them. More dangerous is a "shift,"
when two different viruses mix together to create a radically different strain.
A continual pursuit of virologists is to identify these shifts and drifts each
year in order to develop effective vaccines.
The research was funded by National Institute of Allergy and Infectious
Diseases (NIAID), a component of the National Institutes of Health. "(The
researchers') findings point us in a direction to better understand the
pathology of these more virulent influenza viruses," said Dominick Iacuzio,
program officer for influenza and related viral respiratory diseases at the
NIAID.
For the full text of the article, contact Dave Schneier at the National
Academy of Sciences news office at (202) 334-2138.
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- Brian Mattmiller, (608) 262-9772
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