The least conspicuous strategy of all is to lurk within what’s called a reservoir host. A reservoir host (some scientists prefer “natural host”) is a living organism that carries the pathogen, harbors it chronically, while suffering little or no illness. When a disease seems to disappear between outbreaks (again, as Hendra did after 1994), its causative agent has got to be somewhere, yes? Well, maybe it vanished entirely from planet Earth—but probably not. Maybe it died off throughout the region and will only reappear when the winds and the fates bring it back from elsewhere. Or maybe it’s still lingering nearby, all around, within some reservoir host. A rodent? A bird? A butterfly? A bat? To reside undetected within a reservoir host is probably easiest wherever biological diversity is high and the ecosystem is relatively undisturbed. The converse is also true: Ecological disturbance causes diseases to emerge. Shake a tree, and things fall out.
Nearly all zoonotic diseases result from infection by one of six kinds of pathogen: viruses, bacteria, fungi, protists (a group of small, complex creatures such as amoebae, formerly but misleadingly known as protozoans), prions, and worms. Mad cow disease is caused by a prion, a weirdly folded protein molecule that triggers weird folding in other molecules, like Kurt Vonnegut’s infectious form of water, ice-nine, in his great early novel Cat’s Cradle. Sleeping sickness results from infection by a protist called Trypanosoma brucei, carried by tsetse flies among wild mammals, livestock, and people in sub-Saharan Africa. Anthrax is caused by a bacterium that can live dormant in soil for years and then, when scuffed out, infect humans by way of their grazing animals. Toxocariasis is a mild zoonosis caused by roundworms; you can get it from your dog. But fortunately, like your dog, you can be wormed.
Viruses are the most problematic. They evolve quickly, they are unaffected by antibiotics, they can be elusive, they can be versatile, they can inflict extremely high rates of fatality, and they are fiendishly simple, at least relative to other living or quasi-living creatures. Ebola, West Nile, Marburg, the SARS bug, monkeypox, rabies, Machupo, dengue, the yellow fever agent, Nipah, Hendra, Hantaan (the namesake of the hantaviruses, first identified in Korea), chikungunya, Junin, Borna, the influenzas,
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and the HIVs (HIV-1, which mainly accounts for the AIDS pandemic, and HIV-2, which is less widespread) are all viruses. The full list is much longer. There is a thing known by the vivid name “simian foamy virus” (SFV) that infects monkeys and humans in Asia, crossing between them by way of the venues (such as Buddhist and Hindu temples) where people and half-tame macaques come into close contact. Among the people visiting those temples, feeding handouts to those macaques, exposing themselves to SFV, are international tourists. Some carry away more than photos and memories. “Viruses have no locomotion,” according to the eminent virologist Stephen S. Morse, “yet many of them have traveled around the world.” They can’t run, they can’t walk, they can’t swim, they can’t crawl. They ride.
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Isolating the Hendra bug had been a task for virologists, working in their high- security labs down at AAHL. “Isolating,” in this sense of the word, means finding some of the virus and growing more. The isolate becomes a live, captive population of virus, potentially dangerous if any were to escape but useful for ongoing research. Virus particles are so tiny they can’t be seen, except by electron microscopy, which involves killing them, so their presence during isolation must be detected indirectly. You start with a small bit of tissue, a drop of blood, or some other sample from an infected victim. Your hope is that it contains the virus. You add that inoculum, like a dash of yeast, to a culture of living cells in a nutrient medium. Then you incubate, you wait, you watch. Often, nothing happens. If you’re lucky, something does. You know you’ve succeeded when the virus replicates abundantly and asserts itself sufficiently to cause visible damage to the cultured cells. Ideally it forms plaques, large holes in the culture, each hole representing a locus of virus-caused devastation. The process demands patience, experience, expensively exact bench tools, plus meticulous precautions against contamination (which can falsify results) or accidental release (which can infect you, endanger your co-workers, and maybe panic a town). Laboratory virologists are not generally knockabout people. You don’t meet them in bars, waving their arms and bragging lustily about the perils of their métier. They tend to be focused, neat, and still, like nuclear engineers.
Discovering where a virus lives in the wild is work of a very different sort. It’s an outdoor job that entails a somewhat less controllable level of risk, like trapping grizzly bears for relocation. Now, the people who look for wild viruses aren’t rowdy and careless, no more so than the lab specialists; they can’t afford to be. But they labor in a noisier, more cluttered, more unpredictable environment: the world. If there is reason to suspect that a certain new virus infecting humans is zoonotic (as most such viruses are), the search may lead into forests, swamps, crop fields, old buildings, sewers, caves, or the occasional horse paddock. The virus hunter is a field biologist, possibly with advanced training in human medicine, veterinary medicine, ecology, or some combination of those three—a person who finds fascination in questions that must be answered by catching and handling animals. That profile fits a lanky, soft- spoken man named Hume Field, midthirtyish at the time he became involved with Hendra.
Field grew up in the provincial towns of coastal Queensland, from Cairns to Rockhampton, a nature-loving kid who climbed trees, hiked in the bush, and spent school holidays on his uncle’s dairy farm. His father was a police detective, which seems only too prefigurative of the son’s later role as a viral sleuth. Young Field
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earned an undergraduate degree in veterinary science at the University of Queensland, in greater Brisbane, and volunteered at an animal refuge on the side, helping to rehabilitate injured wildlife. After graduation in 1976, he worked in a mixed veterinary practice in Brisbane for some years and then as a temporary fill-in (the Australians call it “doing locums”) all over the state. During that time, he doctored a lot of horses. But he became increasingly aware that his deepest interest was wildlife, not livestock and pets, so in the early 1990s Field returned to the University of Queensland, this time for a doctorate in ecology.
He focused on wildlife conservation and, in due time, needed a dissertation project. Because feral cats (domestic cats gone wild on the landscape) cause considerable damage to native Australian wildlife, killing small marsupials and birds and acting as a source of disease, he undertook a study of feral cat populations and their impact. He was trapping cats, fitting them with radio collars to track how they lived, when the outbreak occurred at Vic Rail’s stable. One of Field’s doctoral mentors, a scientist who worked with the Department of Primary Industries, asked Field whether he would be interested in changing projects. The department needed someone to investigate the ecological side of this new disease. “So I forgot my feral cats,” Field told me, when I visited him long afterward at the Animal Research Institute, a DPI facility near Brisbane, “and started off looking for wildlife reservoirs of Hendra virus.”
He began his search by going back to the index case—the first equi