Spillover: Animal Infections and the Next Human Pandemic (35 page)

Within a few seconds, Schwarzenegger’s ferocity started to wilt. The animal went clumsy, then limp. Lights out, for at least half an hour.

Working quickly, Engel tried to get each of the others. But it was difficult with six monkeys still ricocheting around the cage and others at his back. He poked a couple more and then reloaded his syringes with Telazol. Nobody wanted to get clawed or bitten. Grab a tail if you can! he hollered to me. Pin one against the mesh! Yeah, right. I made a lame tail-grab attempt, but I was the amateur here, and I found little zeal for exposing my hands to the flying claws and teeth of animals well known for carrying herpes B.

Somehow, within a few minutes, Engel injected all five adults in the trap. When we opened the door, one juvenile and the infant skittered away, but the others were down like drunks.

We loaded them into a duffel bag. Go, go fast, said Engel, and two students carried the bag down the staircase and then hoisted it gingerly over a wall, below which Jones-Engel stood ready to help catch the bundle of doped monkeys. She was dressed in traditional Bangladeshi attire—a camise and salwar pants plus a veil over her shoulders, which was her usual field garb, worn in deference to local sensibilities—but now she also wore exam gloves and a surgical mask. She guided the monkey-bearers down an alley to the private courtyard, where women were welcome, where tables had been prepared, where swabs and vials and clipboards and more syringes had been laid out in readiness. The gathering of data began.

Lisa Jones-Engel is a forceful, direct person with years of experience among Asia’s nonhuman primates. She loves her subject animals but doesn’t romanticize them. As she and her assistants started drawing blood and taking oral swabs, her husband and Feeroz, followed by the male students and me, headed back to the shrine for another round of trapping. Now that we had shown our methods, and our devious intentions, it was dicey to say how the troop might behave. “If the monkeys in the last half hour have figured out their plan of attack,” Lisa commanded us, “you just retreat.”

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“H
erpes B scares the shit out of people,” she told me a few days later. We had returned to Dhaka, and after another long day she and Gregory and I were sharing wee drams of Balvenie in my hotel room. Lisa was adamant. “Herpes B gets populations of monkeys shot in the head and . . .”—she had in mind the safari park culling as well as other such events—“just eradicated. Herpes B is like Ebola that way.” It’s not only frightful and potent, she meant, but profoundly misunderstood.

Herpes B and Ebola, of course, are very different sorts of bug. But she was right; there are similarities worth noting. In both cases, the virus is often lethal to humans but not nearly so consequential as it would be if not constrained by the limits of its transmissibility. It has no preternatural powers. It finds humans a dead-end host. People are ignorant about its actual properties and inclined to imagine an unreal breadth of risk. Among differences between the two, there’s this: Ebola is infamous and herpes B is largely unknown. It’s unknown, that is, unless you work in a monkey lab or run a safari park.

Killing off captive macaques is uncalled for, Lisa insisted, even in populations that might carry the virus, so long as their likelihood of passing it to a human is extremely low. And a positive test for antibodies doesn’t even prove that the virus is still present.

She mentioned a recent case, just three months earlier, in which a research colony of macaques at a university in France was condemned to extermination. Some of those individual animals were known to and studied by attentive ethologists for twenty-five years. The colony was notable for expressing some fascinating behavioral patterns. A thousand primatologists, from the International Primatological Society and other scientific groups, signed petitions challenging the logic of wholesale condemnation. “Look, don’t do this,” they argued. “You don’t really understand what these results mean.” The university council made its decision anyway and, on a Sunday in August, before the scientists and the keepers could protest further, the macaques were all killed.

However dangerous herpes B might be when infecting a person, the chances of monkey-human transmission seem to be extremely small. That’s what those research results from the Sangeh Monkey Forest in Bali suggest. Lisa and Gregory found a high prevalence of the virus among the macaques there, and a high incidence of macaque bites and scratches among the people, but no evidence of herpes B transfer. If cases do sometimes occur in Bali, they must escape medical notice, or else get taken for some other dreadful disease, such as polio, or rabies, which is a serious problem in Bali because of its prevalence among the island’s dogs. Nobody knows whether any undetected herpes B infections have come out of Sangeh. Possibly, none have.

Other data, published almost a decade earlier by a different team, support the impression that herpes B doesn’t leap readily to humans. This study looked at blood samples from 321 laboratory workers—scientists and technicians who handled live primates or else primate cells in culture. Most of those people worked with macaques. Many of them had been bitten, scratched, or splashed. Yet none of the 321 workers tested positive for exposure to herpes B. Evidently the virus is not easily transmitted, and evidently it’s not causing subtle, asymptomatic infections among people in close contact with monkeys.

The medical record notes just forty-three cases, beginning with William Brebner, in which contact between a macaque and a person led to infection. True, those forty-three infections often brought dire results. But over the same period of time, during untold thousands or millions of other such contacts—in laboratories, in the wild, from monkey temples to Petri dishes, via scratching or biting or drool or needlestick accident or splashed urine—herpes B didn’t make the monkey-human leap. Why not? Apparently this virus isn’t ready.

Another way of saying that: Ecology has provided opportunities, but evolution hasn’t yet seized them. Maybe it never will.

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T
he blood drawn from the macaques we trapped at Chashnipeer Majar would be screened for evidence of another virus too. Lisa Jones-Engel and her team had lately shifted their attention to this one. It’s a favorite of mine because of its lurid name: simian foamy virus. No, infected hosts don’t foam at the mouth. The “foamy” part derives from its tendency to cause cells in a host to fuse with one another, forming gigantic, nonfunctional megacells that, under a microscope, resemble bubbles of foam.

There’s actually a whole gaggle of foamy viruses, all lodged within the genus
Spumavirus
. Some of them infect cows, cats, and horses. They have also been found among gorillas, chimpanzees, orangutans, baboons, macaques, and other primates, in each of which they seem to be ancient infections, having coevolved with their hosts for as long as 30 million years, one species of simian foamy virus (SFV) per species of simian. Maybe that’s why, nowadays, they seem so benign. One team working in Central Africa reported evidence of SFV passing from primates that are hunted for bushmeat (mandrills, gorillas, and guenons) into people who hunt those animals. Whether SFV makes the hunters sick is another question, not addressed by that study. If it does, the effects must be slow and subtle. Then again, the HIVs are slow and subtle. And SFV, like the HIVs, is a retrovirus. Jones-Engel isn’t the only researcher who feels that simian foamy virus bears watching.

Thirty years ago, scientists believed that we humans have our own foamy virus, our own endemic version, distinct from the zoonotic foamies we may acquire while feeding rice to a sacred monkey or cutting open a gorilla with our machete. Destructive in cell cultures but apparently harmless in a living person, human foamy virus was called “
a virus in search of a disease
.” Later research with advanced molecular methods—most notably, genetic sequencing—showed that it was probably just a variant of the foamy virus endemic to chimpanzees. Anyway, that one isn’t what interests Lisa Jones-Engel and her husband. They’re more concerned with the versions that dwell in Asian macaques.

Like the African SFVs, those Asian viruses seem to be innocuous when they get into human hosts. During our talk in Dhaka, Lisa stated the point a little more guardedly. “There’s no known disease in nonhuman primates infected with simian foamy virus. Now when the virus jumps the species barrier to humans . . . ”—when that happens, well, it’s hard to say what may occur, because of limited data. “The number of people that we’ve had to look at so far is so small that we really can’t speak yet to whether it does cause disease in humans.” The cases observed have been too few, and the time of observation has been too short. As retroviruses, the SFVs might conceivably have a long, sneaky period of latency and slow replication within the body, before emerging from their secret lairs to wreak havoc.

For Engel and Jones-Engel, this particular line of investigation had its origin at the Sangeh temple, in Bali, where they screened for simian foamy virus as well as for herpes B. And like herpes B, simian foamy seemed to be widespread throughout the population; they found antibodies against it in most macaques tested. A common infection, then, probably passed from monkey to monkey by social contact, again like herpes B. But how often does it spill into humans?

Besides trapping and sampling monkeys, the researchers drew blood from more than eighty people and screened those samples by the same method used for the monkeys. All the humans tested negative except one, a forty-seven-year-old Balinese farmer. This man lived near Sangeh, visited the temple often, and had been bitten once and scratched several times. No, he told them, he had never eaten a monkey. No, he did not keep a pet monkey. If the virus was in him, it must have come from those aggressive animals at the temple. In retrospect, the most notable aspect of what Jones-Engel and Engel found among their eighty-some test subjects in Bali was that
only
the farmer had been infected. Since then, further sampling in other Asian countries (Thailand, Nepal, and Bangladesh) has shown that simian foamy gets into humans more readily than the early results suggested.

But if it causes no known disease, so what?

Beyond the obvious point that it might cause an
unknown
disease, Engel and Jones-Engel have another reason for studying this virus. “It’s a marker,” Gregory told me. “We caught a marker for transmission,” Lisa echoed. What they meant is that the presence of SFV within a human population marks opportunities having occurred for cross-species infection of all kinds. If simian foamy has made the leap from a half-tame macaque to a person—to several people, maybe to thousands of people passing through sites such as Sangeh—then so could other viruses, their presence still undetected, their effects still unknown.

“And why is that important?” I asked.

“Because we’re looking for the Next Big One,” she said.

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T
he Next Big One, as I mentioned at the start of this book, is a subject that disease scientists around the world often address. They think about it, they talk about it, and they’re quite accustomed to being asked about it. As they do their work or discuss pandemics of the past, the Next Big One (NBO) is at the back of their minds.

The most recent big one is AIDS, of which the eventual total bigness (the scope of its harm, the breadth of its reach) cannot even be predicted. About 30 million deaths, 34 million living people now infected, with no end in sight. Polio was a big one, at least in America, where it achieved special notoriety by crippling a man who would become president despite it. Polio also, during its worst years, struck hundreds of thousands of children and paralyzed or killed many, captured public attention like headlights freezing a deer, and brought drastic changes to the way large-scale medical research is financed and conducted. The biggest of the big ones during the twentieth century was the 1918–1919 influenza. Before that, on the North American continent, the big one for native peoples was smallpox, arriving from Spain about 1520 with the expedition that helped Cortez conquer Mexico. Back in Europe, two centuries earlier, it was the Black Death, probably attributable to bubonic plague. Whether the plague bacterium or another, more mysterious pathogen caused the Black Death (as several historians have recently argued), there’s no question of its bigness. Between the years 1347 and 1352, this epidemic seems to have killed at least 30 percent of the people in Europe.

Moral: If you’re a thriving population, living at high density but exposed to new bugs, it’s just a matter of time until the NBO arrives.

Note that most of these big ones but not all of them (plague the exception) were viral. Now that modern antibiotics are widely available, vastly reducing the lethal menace of bacteria, we can guess confidently that the Next Big One will be a virus too.

To understand why some outbreaks of viral disease go big, others go
really
big, and still others sputter intermittently or pass away without causing devastation, consider two aspects of a virus in action: transmissibility and virulence. These are crucial parameters, defining and fateful, like speed and mass. Along with a few other factors, they largely determine the gross impact of any outbreak. Neither of the two is an absolute constant; they vary, they’re relative. They reflect the connectedness of a virus to its host and its wider world. They measure situations, not just microbes. Transmissibility and virulence: the yin and yang of viral ecology.

You’ve heard a bit already about transmissibility, including the simple statement that viral survival demands replication and transmission. Replication can occur only within cells of a host, for the reasons I’ve mentioned. Transmission is travel from one host to another, and transmissibility is the packet of attributes for achieving it. Can the virions concentrate themselves in a host’s throat or nasal passages, cause irritation there, and come blasting out on the force of a cough or a sneeze? Once launched into the environment, can they resist desiccation and ultraviolet light for at least a few minutes? Can they invade a new individual by settling onto other mucous membranes—in the nostrils, in the throat, in the eyes—and gaining attachment, cell entry, another round of replication? If so, that virus is highly transmissible. It goes airborne from one host to another.