Too virulent to spread

My latest Mind and Matter column in the Wall Street Journal is on infleunza:

Here we go again. A new bird-flu virus in China, the H7N9 strain, is spreading alarm. It has infected about 130 people and killed more than 30. Every time this happens, some journalists compete to foment fear, ably assisted by cautious but worried scientists, and then tell the world to keep calm. We need a new way to talk about the risk of a flu pandemic, because the overwhelming probability is that this virus will kill people, yes, but not in vast numbers.

In recent years flu has always proved vastly less perilous than feared. In 1976 more people may have died from bad reactions to swine-flu vaccine than from swine flu. Since 2005, H5N1 bird flu has killed 374 people, not the two million to 7.4 million deemed possible by the World Health Organization. In 2009, H1N1 Mexican swine flu proved to be a normal flu episode despite apocalyptic forecasts.

No doubt some readers will remind me that, in the story of the boy who cried "Wolf!", there eventually was a wolf. And that in 1918 maybe 50 million people died of influenza world-wide. So we should always worry a bit. But perhaps it's not just luck that has made every flu pandemic since then mild; it may be evolutionary logic.

The new virus is said to need just five mutations to turn it into a human-to-human pathogen, two of which have already happened. But evolution is not just about mutation; it is also about selection. Assuming that a virus acquires the capacity to spread from person to person, will its virulence rise or fall as it spreads? As Maciej Boni of Oxford University and his colleagues argue in a new paper, this is an evolutionary question, because the change will come about through the relative success of different genetic strains.

Imagine you are a flu virus. Your job is to see your progeny—copies of your genome—safely into as many new people as possible. There's competition from other mutant versions. Would you rather have your victim lying on his deathbed or out and about meeting people, albeit with a headache and a cough?

In casual-contact diseases, there is a general tendency for virulence to decline. Colds are caused by hundreds of kinds of virus, none of which has ever been seriously lethal. Mosquito-borne diseases, by contrast, benefit from making their victims so ill that they lie still in darkened rooms perspiring and attracting insects.

Why was flu so lethal in 1918? Perhaps the peculiarly crowded and intimate conditions of the trenches and field hospitals of World War I suited a high-virulence flu, though nobody can be sure. Jeffery Taubenberger of the Armed Forces Institute in Rockville, Md., and David Morens of the National Institutes of Health in Bethesda argued in a recent paper that the virus was essentially novel and that all subsequent flu pandemics consist of its low-virulence genetic descendants, sometimes with added genes from other strains. It was indeed "the mother of all pandemics."

Calculations by Dr. Boni and his colleagues show that with 60% mortality, H5N1 bird flu is still four times too lethal to be able to spread within a human population. In captive ferrets (the experimental animal of choice for flu research) it is rapidly evolving toward lower virulence. Ironically, the most worrying sign for a bird-flu pandemic would be if the virulence dropped significantly—then it could spread. There are signs this might be happening in Egypt.

There's no mystery as to why we talk up the risk every time: All the incentives point that way. Who among the headline-seeking journalists, reader-seeking editors, fund-seeking scientists, contract-seeking vaccine makers or rear-end-covering politicians has even a modest incentive to say: "It may not be as bad as all that"?