December 30, 2011 | 17
A controversy over whether the U.S. government should allow details of a deadly new flu strain to be published in scientific journals has recently caught fire in the media. But I first heard the news of the mutated virus months ago in Malta at the European Scientific Working group on Influenza (ESWI) meeting.
The morning was sunny and warm on September 12 in St. Julian’s. Inside the Intercontinental hotel and conference center, young researchers, jaded veteran scientists and jet-lagged policy makers piled their plates with softly scrambled eggs, American-style sausages and an obligatory piece of fruit or two, shoveling in the offerings and mumbling hellos, in the bright, sky-lit hotel restaurant.
Just across the hall, however, in the cannily named Eden Arena, the room was dark, as researchers prepared to mount the stage and explain some of the many ways that humanity might soon be threatened by a truly terrifying flu pandemic.
So maybe it wasn’t quite that dramatic, but perhaps it should have felt more so. Less than an hour later, a suspiciously sniffly Ron Fouchier, a lanky virologist from the Erasmus Medical Center in Rotterdam with a wry smile and reassuringly understated manner, would announce that he and his lab had found a way to make the deadly H5N1 that would likely be just as transmissible from one human to the next as the seasonal flu.
Circulating seasonal strains, such as H3N2, are adept at attaching to the human nasal cavity and trachea, making them easily transferable among people via a sneeze, cough or sigh. But fortunately for us, H5N1, as it has circulated in bird populations, has not yet developed this capability. Fouchier and his team wanted to see if it was possible to give it that power.
So they “mutated the hell out of H5N1,” Fouchier said, towering over the podium at the meeting’s Monday morning plenary session. But as it turns out, they hardly needed to. With just a few genetic substitutions, the virus was able to affix to nose and trachea cells—a development “which seemed to be very bad news,” he said. Fortunately for the lab’s test ferrets, a common animal model for human flu transmission, the flu still didn’t seem to pass airborne from animal to animal.
And that was when “someone finally convinced me to do something really, really stupid,” Fouchier recounted. They put the mutated H5N1 into the nose of one ferret, then took a sample of nasal fluid from that ferret and put it in the nose of another. After 10 ferrets, the virus began spreading from ferret to ferret via the air just about as easily as a seasonal flu virus.
In all that ferret hopping, the virus gained only five new genetic substitutions. And that was also “very bad news,” Fouchier proclaimed, adding an “indeed” for emphasis, just in case the ramifications were lost on any of the hundreds of flu folks in the audience.
At the time, Fouchier declined to specify the exact locations of the mutations but noted that the key substitutions are in the HA and PB2 areas. All of the mutations needed to make the virus an airborne threat have already been detected in the wild, but they have not been found together in a single virus “just yet,” Fouchier noted. The discovery also confirmed that H5N1 would not need to mingle with a mammalian virus before becoming easily transmissible among us.
H5N1 has killed about half of the people who have gotten it (most were likely infected directly from contact with fowl—hence its common nickname, bird flu). For comparison, the 1918 influenza pandemic strain of H1N1 killed between 10 and 20 percent of those who caught it.
“This is a very dangerous virus,” Fouchier said, posing the question so many in the audience had surely been mulling over: “Should these experiments be done?” His answer was cool “yes.” He defends his lab’s work, which was funded by grants from the U.S. government, and he has spent the past weeks reassuring interviewers that the virus is closely controlled. “It’s important that we keep working with these viruses,” he said. And he advocates that the findings have an important power to “send out the message that H5N1 could become airborne,” he said. And that knowledge should spur scientists and policy makers alike to work harder to develop better vaccines and try to eradicate it in the wild.
The virus itself already kills—or necessitates the culling of—millions of chickens in Asia each year, which can be a huge economic hit to local farmers. To say nothing of the danger that each new infection—in human or fowl—ups the odds that these mutations will come together on their own. Knowing which mutations are needed to make H5N1 transmissible among humans could put scientists and those in charge of tracking the virus on closer watch for any of them when they appear in the wild.
At a reception the next evening in Malta, Maria Van Kerkhove, of the Imperial College London’s School of Public Health, told me that from a scientific perspective, she thought this particular recombination has a “low probability” of occurring. But given its exceedingly high mortality rate it’s a “really high-impact thing to prepare against—it’s like preparing against terrorism.”
But that was the end of the terrorism talk—a threat that has repeatedly been raised in arguments against publication of the full findings in Science and Nature (Scientific American is part of Nature Publishing Group). The scientists at the ESWI meeting seemed already in agreement with a concept recently articulated by the film Contagion, released earlier that month. As Laurence Fishburne’s character, an infectious disease expert in the movie says: “Someone doesn’t have to weaponize the bird flu—the birds are already doing that.” Only in the real life case these days, we’re fixated on ferrets. Fluish ferrets—and a switch-by-switch map of the mutated virus—or not, a nefarious influenza plot seems unlikely. Without a vaccine and with such quick and frequent global travel, any group unleashing such a deadly virus would eventually wind up putting half of their own at risk as well.
12 Digital Issues + 4 Years of Archive Access just $19.99X