Deadly Flu, or Chicken Little Syndrome?
THERE’S A HIDDEN WAR ON terror taking place, literally under our noses. Call it the war on microterror: Our own versions of the Department of Homeland Security, human antibodies, are fighting off a steady barrage of foreign threats such as viruses and bacteria. In this war, one of today’s most feared weapons of mass destruction is avian flu. President Bush has launched a multibillion-dollar initiative to prepare for the response. But avian flu has been around seven years and does not yet readily spread from person to person, raising questions about whether the threat is being overblown.
Those who say the threat is real—and they are in the majority—point out that the virus—called H5N1, or hemagglutinin type 5 and neuraminidase type 1—is highly mutable, which means it could quickly morph into a human contagion or merge with one, yielding an organism that is both deadly and can spread among humans.
In the “it’s not a matter of if, but when” camp is Gilbert Smolin, M.D., a clinical professor at the University of California-San Francisco and a lecturer on infectious diseases. “This one is scary because it’s spreading so fast and is so lethal to humans,” Smolin says. Half of the approximately 140 human victims have died.
But there’s another way to look at the numbers, says Alan P. Zelicoff, M.D., a physician and physicist as well as a former senior scientist at Sandia National Laboratories. For example, he estimates that during the seven years that H5N1 has been around—which he calls an “eon” for a highly mutable virus—people have had interactions with sick birds billions of times, resulting in some 140 cases of human infection, most of them in Vietnam.
Zelicoff further notes that the deadly 1918 Spanish flu pandemic, which went from chickens to humans, then from human to human, is a far cry from today’s situation. “It is tempting to a biologist to say a mutation looks like 1918,” he says, because they’ve seen changes in one major protein on the surface of the virus that resembles what happened with the 1918 flu. But perhaps 10 more critical amino acid changes in that protein would still need to occur for the comparison to the 1918 flu to be more apt.
Even if those changes did occur, the H5N1 virus doesn’t live long, and would need another “willing host” very close by. That’s what happened in 1918, Zelicoff says, when soldiers with compromised immune systems were packed into trenches, ships, boot camps, and military hospitals. The virus further spread in densely packed tenements, where families huddled together in one room for warmth, he adds.
Some experts fear that today’s avian flu is transmittable when people pack together in subways, stadiums, and similar places. But they’re not together for days at a time, Zelicoff says. Plus, heat and UV rays kill off the virus, and in the United States, “even in the worst slums, there’s central heating.”
Another consideration is how well people’s immune systems could fight back. Smolin and many other experts say that H5N1 is so deadly because no one has antibodies to it. Whether people need antibodies resistant to that exact strain is a matter of contention, however.
Zelicoff says that antibodies to either H5 or N1—not both—confer resistance. And most Westerners have N1 antibodies because they are a component of flu shots or because they’ve gotten a virus with an N1 component. According to Zelicoff, his theory is borne out by the fact that many of the victims of avian flu have been children—and they are the people most likely not to have been vaccinated or to have developed a resistance to N1.
Is a deadly outbreak inevitable? Smolin and others say yes, but Zelicoff counters that it’s more likely that he personally will be hit by a meteor. “It’s so unlikely that we have much better places to spend the $7 billion that the President has proposed,” he says.
