The Viral Storm (11 page)

Nipah virus was first detected in Malaysia, in the village that gave it its name. This virus kills. Of the 257 cases of infection seen during 1999 in Malaysia and Singapore, 100 people died, a startlingly high mortality rate. Among the survivors, more than 50 percent were left with serious brain damage.

The first clues to the origin of the virus were the patterns of human cases. The vast majority occurred among workers in piggeries. At first, the investigators thought the virus causing the illness was Japanese encephalitis virus, a mosquito-borne virus present throughout tropical Asia. Yet menacing and distinct symptoms led the investigating teams to determine that it must be a new and still unidentified agent.

Early symptoms of Nipah virus include those common in viral infections—fever, decreased appetite, vomiting, and flu-like systems. But after three to four days, more serious nervous system manifestations appear. The exact impact that the virus has differs from person to person. Some individuals experience paralysis and coma, while others have hallucinations. One of the first documented patients reported seeing pigs running around his hospital bed.

MRI scans show serious damage to patches of the brain, and the patients who die usually do so within a few days of the onset of brain damage. Among the individuals infected in Malaysia and Singapore in 1999, none appeared to seed additional human infections, yet cases in subsequent years in Bangladesh provide evidence that the virus has the potential to spread from human to human under at least some circumstances.

*   *   *

When scientists discover a new virus, a mad rush often ensues to identify the
reservoir
of the virus—the animal that maintains it. While certainly useful, the concept of a reservoir also has limitations. Scientists often see stark divisions between species. We neatly divide up the world of animals into families, genera, and species, but we often forget that these divisions are based on our own conventions. A taxonomist can clearly sort out the difference between a colobus monkey, a baboon, a chimpanzee, a gorilla, and a human, yet the traits that permit us to classify these animals as distinct are, as I’ve mentioned, often irrelevant for a microbe. From the perspective of a virus, if cells from distinct species share the appropriate receptors, and ecological connections provide the appropriate opportunities to make a jump, the fur of a baboon or the upright status of a human does not matter at all.

Some viruses persist permanently and simultaneously in multiple hosts. Dengue virus, a viral infection originally called breakbone fever because of the intense pain it causes, appears largely in human cities. Yet dengue also lives in wild primates in tropical forests, where it is referred to as sylvatic dengue.
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Sylvatic dengue simultaneously infects multiple species of primates and does not discriminate. It has a wide
host range
.

Among the numerous dry technical scientific papers that I digested as a doctoral student, few are indelibly etched on my brain. One that I remember in detail was a report describing experiments to determine the host range of sylvatic dengue.

In the study, which used outdated methods now considered unethical, scientists put various species of primate into cages and used ropes to lift the cages high into the canopy where dengue’s forest mosquitoes feed. There they gathered samples of viruses to determine which species had the potential for infection. The study largely worked—except in one case where they brought the cage down only to find a massive python with a very badly distended abdomen. The large snake had entered the cage to consume the trapped and no doubt terrified monkey. Having miscalculated, the satiated snake could not squeeze through the bars to escape and found itself in the same trapped predicament as its monkey prey. Most likely the snake didn’t get infected with the virus; few viruses infect both reptiles and mammals. It did, however, make for a memorable photo in an otherwise dry technical journal.

Image from the sylvatic dengue study.
(
Institute of Medical Research Malaysia / A. Rudnick, T. Lim
)

The capacity for sylvatic dengue to thrive in multiple species presumably helps the virus persist in regions where the population density of any single primate species would not be sufficient to protect the virus from extinction. And the mechanism dengue uses to move from one animal to another—mosquitoes—helps make this movement seamless.

*   *   *

For dengue, the notion of a single reservoir does not, strictly speaking, make sense, but when Nipah was discovered in 1999, that was still unclear. Scientists then asked themselves: what local animal or animals, wild or domestic, were Nipah’s reservoir? Knowing what animal or animals a virus lives in prior to infecting humans helps us respond to it. Depending on the reservoir, we may have the potential to simply change farming practices or modify human behavior to avoid the critical contact that leads to viral exchanges, effectively cutting off the virus’s ability to enter humans.

Knowing that a microbe has the capacity to maintain itself in an animal reservoir also changes the way that we think about public health strategies. Microbes can jump in both directions, so while novel human microbes like Nipah originate in animals, established microbes also have the potential to cross back into animals. Animal reservoirs for established human bugs can potentially derail control efforts. In effect, if we eliminate a bug in humans in a particular region, but it lives on in animals, the microbe may have the potential to reemerge with deadly consequences. In order to truly eradicate a human pathogen, we must know if it can also live outside of humans.

When Nipah emerged in 1999, the scientists studying it moved quickly to home in on its reservoir. Over the years that followed, an intricate relationship among wild animals, domesticated animals, and plants revealed itself, a story that emphasizes the complex ways that domestication can provide new avenues for bugs to pass into people.

The Malaysian piggeries that Nipah entered are not small-scale affairs. They house thousands of pigs at very high densities, creating a ripe environment for viral spread. The farmers who raise the pigs work hard to maximize their income both from the pigs themselves, but also from the surrounding land. One of the practices in this area of southern Malaysia is to grow mango trees in and around piggeries, providing a second source of income to increase the viability of the farming enterprise.

In addition to producing delicious fruit for the farmers to sell, the mango trees attract the flying fox, a large and appropriately named bat with the scientific name
Pteropus
. This bat was the unexpected Nipah reservoir, the virus’s link to the wild. Remarkably, it now appears that the
Pteropus
bats, while consuming their mango suppers, urinate and drop partially eaten mango into the pig pens. The omnivorous pigs consume the Nipah-infected bat saliva and urine as they eat the mango. The virus then spreads quickly in the dense pig populations, which, because the animals are sometimes shipped from place to place, infect new piggeries and occasionally infect their human handlers.
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Wahlberg’s Epauletted Fruit Bat (
Epomophorus wahlbergi
) eating mango.
(
Dr. Merlin D. Tuttle / Bat Conservation International / Photo Researchers, Inc.
)

Emerging thousands of years after the advent of domestication, Nipah illustrates the impact that domestication had on our relationship with microbes. The larger and more sedentary populations of humans that emerged following the domestication revolution were susceptible to outbreaks in ways that our predomestic ancestors never were. In the small mobile communities that dominated human life prior to agriculture, novel microbes that entered these communities from animals would often sweep through, killing certain individuals and leaving the rest of the small populations immune. At that point the viruses would effectively die out; a virus without a susceptible host is unable to survive.

As villages and towns formed around agricultural centers, they did not do so in isolation. Communities were connected, at first with footpaths, then roads. While we might think that these towns were separate functional entities, from the perspective of a microbe, they represented a single larger community. As this interconnected community of towns grew, it provided the first opportunity in human history for an acute virus to persist permanently in the human species.

*   *   *

Chronic viruses that live permanently within their hosts, like hepatitis B, do not necessarily require large populations because they can continue to pass on their progeny for many years. These viruses have the potential to persist in very small communities, taking a long-term strategy—he who fights and hides away lives to fight another day. On the other hand, acute viruses, such as measles, do not remain in a single individual for long and require a constant supply of susceptible hosts. As they burn through populations, they kill some and make the rest immune, often leaving no one to perpetuate the infection.

Therefore, within the small, mobile hunter-gatherer lifestyle that our ancestors led prior to domestication, acute viruses could not survive for long unless they were microbes that we shared with other species. In the same way, chimpanzee populations, including those that were studied by the pioneering primatologist Jane Goodall, have sometimes been hit with polio. The virus that causes polio normally requires large populations of contemporary humans to sustain itself. Nevertheless, in 1966 Dr. Goodall and her colleagues saw that the wild chimpanzees they studied had come down with something that looked very much like human polio, including symptoms of flaccid paralysis. The outbreak was devastating for the chimpanzee community in Tanzania, killing a number of animals.

The virus that caused chimpanzee polio was in fact the same virus that caused polio in humans. It had jumped over
from
nearby humans who were experiencing an outbreak at the same time. Dr. Goodall and her colleagues administered vaccine to the chimpanzees, which no doubt limited the harm to the community. Chimpanzees, like our early human ancestors prior to domestication, would not have had the population sizes to maintain such a virus—current estimates suggest that communities of over 250,000 people are necessary to sustain it. In small communities, the virus would simply have swept through, harming some and creating immunity in the others, before dying out.

But when our ancestors, with their farms and domestic animals, began to have interconnected towns, viruses like polio gained the ability both to infect us and to be maintained within our species. As more and more towns appeared and the connections between them improved, the number of people in contact with each other increased. From the perspective of a microbe, the physical separation of these towns didn’t matter if there were enough people moving between the towns. Hundreds, and later thousands, of interconnected towns effectively became a single megatown for microbes. Eventually, the number of interconnected people would become so large that viruses could maintain themselves permanently. As long as new people entered into the populations through birth or migration, and did so with enough frequency, there would always be a new person for the microbe to try.

*   *   *

In effect, domestication provided a triple hit to our ancestors when it came to microbes. It provided sufficiently close contact with a small set of domesticated animals, allowing their microbes to cross over into us. At the same time, domestic animals provided a regular and reliable bridge to wild animals, giving their microbes increased opportunities to cross into us. Finally, and perhaps most crucially, it permitted us to have large and sedentary communities that could sustain microbes that previously would have been a flash in the pan. Together, this viral hat trick put us in a new microbial world—one that would lead, as we’ll see in the next chapter, to the first pandemic.

PART II

THE TEMPEST

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