those might be as nasty as NPV. So . . . what’s the prognosis? Is it valid, The Analogy? Should we expect to crash like a population of gypsy moths?
Dwyer couldn’t be rushed into saying yes. Judiciously empirical, wary of easy extrapolations, he wanted to pause and think. He did. And then we found ourselves talking about influenza.
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I haven’t said much about influenza in this book, but not because it isn’t important. On the contrary, it’s vastly important, vastly complicated, and still potentially devastating in the form of a global influenza pandemic. The Next Big One could very well be flu. Greg Dwyer knew this, which is why he mentioned it. I’m sure you don’t need reminding that the 1918–1919 flu killed about 50 million people; and there’s still no magical defense, no universal vaccine, no foolproof and widely available treatment, to guarantee that such death and misery don’t occur again. Even during an average year, seasonal flu causes at least 3 million cases and more than 250,000 fatalities worldwide. So influenza is hugely dangerous, at best. At worst, it would be apocalyptic. I’ve left it for now only because it’s well suited to suggest some closing thoughts on the whole subject of zoonotic disease.
First, the basics. Influenza is caused by three types of viruses, of which the most worrisome and widespread is influenza A. Viruses of that type all share certain genetic traits: a single-stranded RNA genome, which is partitioned into eight segments, which serve as templates for eleven different proteins. In other words, they have eight discrete stretches of RNA coding, linked together like eight railroad cars, with eleven different deliverable cargoes. The eleven deliverables are the molecules that comprise the structure and functional machinery of the virus. They are what the genes make. Two of those molecules become spiky protuberances from the outer surface of the viral envelope: hemagglutinin and neuraminidase. Those two, recognizable by an immune system, and crucial for penetrating and exiting cells of a host, give the various subtypes of influenza A their definitive labels: H5N1, H1N1, and so on. The term “H5N1” indicates a virus featuring subtype 5 of the hemagglutinin protein combined with subtype 1 of the neuraminidase protein. Sixteen different kinds of hemagglutinin, plus nine kinds of neuraminidase, have been detected in the natural world. Hemagglutinin is the key that unlocks a cell membrane so that the virus can get in, and neuraminidase is the key for getting back out. Okay so far? Having absorbed this simple paragraph, you understand more about influenza than 99.9 percent of the people on Earth. Pat yourself on the back and get a flu shot in November.
At the time of the 1918–1919 pandemic, no one knew what was causing it (though there were plenty of guesses). No one could find the guilty bug, no one could see it, no one could name it or comprehend it, because virology itself had scarcely begun to exist. Techniques of viral isolation hadn’t yet been developed. Electron microscopes hadn’t yet been invented. The virus responsible, which turned out to be a variant of H1N1, wasn’t precisely identified until . . . 2005! During the intervening decades there were other flu pandemics, including one in 1957, which killed roughly 2 million people, and another in 1968, which became known as the Hong Kong flu (for where it began) and killed a million. By the end of the 1950s, scientists had recognized the influenza viruses as a somewhat mystifying group, highly diverse and variously capable of infecting pigs, horses, ferrets, cats, domestic ducks, and chickens as well as people. But no one knew where these things lived in the wild.
Were they zoonoses? Did they have reservoir hosts? One hint appeared in 1961, when a number of common terns (Sterna hirundo, a kind of seabird) died in South Africa and were found to contain influenza. If the flu virus had killed them, then by definition the terns weren’t its reservoir; but maybe their life histories put them in contact with the reservoir. Soon after that, a young biologist from New Zealand went for a walk along the coast of New South Wales with a young Australian biochemist. They saw some dead birds.
These two men were great pals, sharing a love for the outdoors. Their beach walk, in fact, was part of a fishing trip. The New Zealander was Robert G. Webster, transplanted to Australia to do his PhD, and the Australian was William Graeme Laver, educated in Melbourne and London, inspired to