The Flu Hunters

When a mysterious and deadly flu virus struck Hong Kong last year, medical detectives from around the world, fearing a repeat of the 1918 epidemic that killed more than 20 million, sprang into action.

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It was March of 1997 when the chickens began to die--6,800 on three farms in Hong Kong's rural New Territories. Because poultry is a vital part of Hong Kong's diet, agricultural authorities got concerned and quickly consulted Kennedy Shortridge, a microbiologist at the University of Hong Kong. He in turn contacted his friend and fellow flu specialist Robert Webster of St. Jude. For decades both men had studied influenza viruses in chickens and other birds in the belief that these viruses were more than just an agricultural problem and might hold the key to the origins of human influenza, possibly even the virus of 1918.

Shortridge and Webster immediately recognized the gravity of the chicken-flu outbreak in Hong Kong, at least for the region's chicken industry. They knew that while avian influenza did not ordinarily make its host sick, a benign virus could reassort to produce a pathogen of almost inconceivable lethality. Webster's Memphis lab had observed such a transformation in the wild on two occasions, the first in April 1983, when a relatively mild influenza struck chickens on the vast chicken farms of Pennsylvania. The birds got visibly sick, some died and egg production fell, but overall the outbreak remained only a vexing economic problem.

By October, the virus had changed. Before, it attacked the respiratory and intestinal tracts of chickens; now, suddenly, it assaulted every tissue in the chickens, including the brain. It caused all their blood vessels to leak and killed them within days, turning the birds, as one researcher put it, into "bloody Jell-O." Federal inspectors arriving at Pennsylvania farms found themselves walking through factory-size chicken coops struck eerily silent, with thousands of dead or hemorrhaging chickens at their feet. The U.S. Department of Agriculture ordered the extermination of 20 million chickens in Pennsylvania, more than 10 times the number that would be killed in the Hong Kong chicken slaughter.

Webster assigned a young scientist, Yoshihiro Kawaoka, to try to figure out how the virus transformed itself into such a "hot" pathogen. Kawaoka, now a professor of virology at the University of Wisconsin, Madison, compared the genetic structure of viruses from the first and second waves and found only a single, extremely subtle change in the H gene. The two viruses differed by just one nucleotide--one of 1,700 nucleotides that made up the gene.

Last year, on two of the three farms stricken in Hong Kong, mortality was 100%. The scientists knew the virus had a variation of the H gene known as H5--one that is notoriously lethal to chickens. Shortridge did briefly wonder if the virus might eventually cause problems for humans. In an earlier study, conducted with great discretion, his lab had found that residents of rural Hong Kong had antibodies to all the known bird-flu viruses. What that suggested, says Shortridge, was that "any virus could cross the species barrier to humans. But whether it could set up an infection, be established as an infection and maintained as an infection is, of course, another matter."

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