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Why influenza keeps failing to live up to pessimistic forecasts

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

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

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

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

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

By Matt Ridley | Tagged:  rational-optimist  wall-street-journal