Science and news cycles sometimes converge in unhandy ways. That was the case on on January 1, when word came out of Shenzen, a Chinese city bordering Hong Kong, that a 39-year-old bus driver, surnamed Chen, had died of the H5N1 (or bird flu) virus.
The deeply personal tragedy for Chen and his family ought not to be such scary news for most other folks. Since 2003, there have been only 573 confirmed cases of H5N1, according to the World Health Organization (WHO), and though 60% of the victims have died, that’s still a vanishingly tiny number of people in a global population of 7 billion. As long as the H5N1 virus doesn’t jump easily from person to person — which it manifestly does not — it will remain a danger only to those who happen to come in contact with infected poultry.
So little cause for worry, right? Not quite. Because less than two weeks ago, scientists also revealed that they had engineered a strain of bird flu that does make the jump among humans — or at least makes the jump between ferrets, which serve as good models for how humans become infected. The risk is not just that the virus could escape the lab, leading to some cheesy but not-so-implausible Michael Crichton-type sic-fi horror. Rather, the far more realistic risk is that the virus could fall into the hands of bioterrorists, who could unleash a flu pandemic similar to the 1918 Spanish flu that killed 50 million people. This danger is real enough that the U.S. National Science Advisory Board for Biosecurity (NSABB) took the unprecedented step of asking the journals Science and Nature not to publish their reports of the work — or at least to redact enough material to make it impossible for the bad guys to replicate the virus.
The seemingly pointless viral tinkering that led to the new H5N1 strain actually did have a point. Only by knowing exactly what an H5N1 virus looks like as it mutates into one that humans could transmit to one another can scientists recognize when the same mutations are occurring in wild viruses. That sensible reasoning likely won’t stop people from seeing a cause-and-effect between the engineered virus and the Shenzen death — and blaming the researchers who did the recent work. They shouldn’t.
The death of the Chinese bus driver is likely the influenza equivalent of the case of Hannah Poling, the now 13 year old girl who developed autism in 2000 after receiving an atypically large cluster of nine vaccines in an atypically short stretch. Ah-ha! the Jenny McCarthys of the word said, vaccines do cause autism. In this exceedingly unusual case, they apparently did contribute to the girl’s condition — but only because she suffered from an uncommon mitochondrial disorder that, in the presence of such a big vaccine dosing, led to developmental damage. The larger link between the inoculations and autism remains completely nonexistent.
In the current H5N1 case, there is even less to suggest a connection between the engineered virus and the death in Shenzen. There is absolutely no evidence of any kind that the virus, jointly created by scientists at the University of Wisconsin in Madison and Erasmus University in Rotterdam, escaped either lab, much less made its way to China. Meantime, there is plenty to suggest that wild bird flu was at large in China.
Less than a week ago, two birds tested positive for H5N1 in Hong Kong, leading to a temporary ban on imports and sales of live poultry in the region, not to mention the slaughter of 19,000 potentially infected birds. Those are exactly the steps that should be taken to control a possible contagion, though they are not a guarantee that no one — a 39-year-old bus driver named Chen, for example — will get sick.
The current emergency should pass in Hong Kong and Shenzen, and Chen’s family will deeply mourn his loss. Meantime, the rest of us can go on reasonably debating the risks and rewards of mucking about with lethal viruses — a legitimate discussion, as long as we don’t get distracted by tragic coincidences.