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May 14, 2009 - Just weeks after scientists said they had a new drug able to prevent or cure any type A flu, the type A H1N1 swine flu came out of nowhere.
It's offering scientists a once-in-a-lifetime, real-world test of their prediction that all of the more dangerous type A flu viruses share a common Achilles heel -- and that their antibody-based treatment can prevent or cure infection with any pandemic or seasonal type A flu bug.
"For a scientist, to have a potential pandemic strain come out just after an observation like this is phenomenal," Wayne Marasco, MD, PhD, tells WebMD. "You jump up and down, but at the same time you recognize the severe significance of this for public health. I don't want anyone to get sick."
If the new flu bug fits the pattern, Marasco and his colleagues may end up preventing a lot of sickness.
Marasco, a researcher at Dana-Farber Cancer Institute and Harvard Medical School, made the discovery along with Ruben Donis, PhD, chief virologist at the CDC; Robert Liddington, DPhil, director of infectious diseases at La Jolla's Burnham Institute; and others.
The discovery -- made almost accidentally while searching for a way to neutralize the H5N1 bird flu -- was that all type A flu bugs have a shared vulnerability.
The "H" part of the flu bug is the hemagglutinin or HA protein on the outer coat of the virus. That's the part of the virus targeted by immune responses and by traditional flu vaccines.
There are 16 different known HA proteins -- and each one changes its genetic structure at the drop of a hat. This is why flu vaccines have to be changed so frequently.
The HA protein is shaped like a lollipop, and its most changeable parts are in the globular "candy" top. But the target Marasco and colleagues found is on the stem of the lollipop, which doesn't change much. In fact, there are only two, very closely related versions of the target. This means that the 16 HA flu types -- each with with multiple variations -- can be reduced to two basic flu types.
Marasco and colleagues genetically engineered human monoclonal antibodies that block both lollipop-stem targets. The antibodies inactivated every flu bug they could find.
"And it gets even better than that," Marasco says. "If the virus can readily undergo genetic changes in this globular head, why shouldn't it be able to undergo changes in this stem? And it cannot. ... When we tried to make escape mutations; the virus fell apart. And when we tried to ask the virus to escape the antibody, it couldn't do it."
If the new drug works, so what? Can a new, high-tech drug really be made available to the people who most need it?