Scientists Race To Head Off Lethal Potential Of Avian Flu
By David Brown
Washington Post Staff Writer
Tuesday, August 23, 2005; Page A01
Robert G. Webster is watching his 40-year-old hunch about the origin of pandemic influenza play out before his eyes. It would be thrilling if it were not so terrifying.
Four decades ago, Webster was a young microbiologist from New Zealand on a brief sojourn in London. While he was there, he did an experiment that pretty much set the course of his scientific career. In just a few hours, he showed that the microbe that swept the globe in 1957 as "Asian flu" bore an unmistakable resemblance to strains of virus carried by certain birds in the years before.
Webster's observation was a surprise -- and a troubling one. It suggested an origin of the unusually virulent strains of influenza virus that appear two or three times each century. His hunch, that at least some of these pandemic strains were hybrids of bird and human flu viruses, was correct.
Since then, Rob Webster has become arguably the world's most important eye on animal influenza viruses. These days, he is deeply worried about what he's seeing.
Strains of influenza virus known as A/H5N1 have been spreading in wild and domestic birds across Southeast Asia and China since 1996. In recent weeks, the virus has apparently struck poultry in Siberia and Kazakhstan.
Since late 2003, about 100 million domesticated birds -- mostly chickens and ducks -- either have died of the virus or have been intentionally killed to keep the viruses from spreading. But what has Webster and other experts so worried are the 112 people who have been infected with the H5N1 "bird flu," more than half of whom have died. The fatality rate of 55 percent outstrips any human flu epidemic on record, including the epochal Spanish flu of 1918 and 1919 that killed at least 50 million people.
Why this new virus is so deadly is not entirely understood, although scientists have hints.
Influenza viruses invade cells lining the throat and windpipe, where they replicate and cause inflammation but are eventually suppressed by the immune system. In some cases, the microbe invades the lungs and leads to viral or bacterial pneumonia. Some H5N1 strains, however, have two features that make them even more dangerous.
Normally, the flu viruses can replicate only in the throat and lungs. With H5N1, however, the protein that triggers replication can be activated in many other organs, including the liver, intestines and brain. What is usually a respiratory infection can suddenly become a whole-body infection. Simultaneously, a second "defect" in the virus unleashes a storm of immune-system chemicals called cytokines. In normal amounts, cytokines help fight microbial invaders. In excessive amounts, they can cause lethal damage to the body's own tissues.
The trait H5N1 has not acquired is the ability to spread easily from person to person. The 112 human cases since late 2003 may turn out to be simply rare events in a bird epidemic that will eventually subside, as all epidemics do.
What is worrisome, though, is evidence pointing the other way.
Washington Post Staff Writer
Tuesday, August 23, 2005; Page A01
Robert G. Webster is watching his 40-year-old hunch about the origin of pandemic influenza play out before his eyes. It would be thrilling if it were not so terrifying.
Four decades ago, Webster was a young microbiologist from New Zealand on a brief sojourn in London. While he was there, he did an experiment that pretty much set the course of his scientific career. In just a few hours, he showed that the microbe that swept the globe in 1957 as "Asian flu" bore an unmistakable resemblance to strains of virus carried by certain birds in the years before.
Webster's observation was a surprise -- and a troubling one. It suggested an origin of the unusually virulent strains of influenza virus that appear two or three times each century. His hunch, that at least some of these pandemic strains were hybrids of bird and human flu viruses, was correct.
Since then, Rob Webster has become arguably the world's most important eye on animal influenza viruses. These days, he is deeply worried about what he's seeing.
Strains of influenza virus known as A/H5N1 have been spreading in wild and domestic birds across Southeast Asia and China since 1996. In recent weeks, the virus has apparently struck poultry in Siberia and Kazakhstan.
Since late 2003, about 100 million domesticated birds -- mostly chickens and ducks -- either have died of the virus or have been intentionally killed to keep the viruses from spreading. But what has Webster and other experts so worried are the 112 people who have been infected with the H5N1 "bird flu," more than half of whom have died. The fatality rate of 55 percent outstrips any human flu epidemic on record, including the epochal Spanish flu of 1918 and 1919 that killed at least 50 million people.
Why this new virus is so deadly is not entirely understood, although scientists have hints.
Influenza viruses invade cells lining the throat and windpipe, where they replicate and cause inflammation but are eventually suppressed by the immune system. In some cases, the microbe invades the lungs and leads to viral or bacterial pneumonia. Some H5N1 strains, however, have two features that make them even more dangerous.
Normally, the flu viruses can replicate only in the throat and lungs. With H5N1, however, the protein that triggers replication can be activated in many other organs, including the liver, intestines and brain. What is usually a respiratory infection can suddenly become a whole-body infection. Simultaneously, a second "defect" in the virus unleashes a storm of immune-system chemicals called cytokines. In normal amounts, cytokines help fight microbial invaders. In excessive amounts, they can cause lethal damage to the body's own tissues.
The trait H5N1 has not acquired is the ability to spread easily from person to person. The 112 human cases since late 2003 may turn out to be simply rare events in a bird epidemic that will eventually subside, as all epidemics do.
What is worrisome, though, is evidence pointing the other way.
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