Crisis in the Hot Zone

By Richard Preston

The main building of the United States Army Medical Research Institute for Infectious Diseases is an essentially windowless concrete block that covers several acres at Fort Detrick, an Army base in Frederick, Maryland, fifteen miles east of Antietam. Military people call the structure the Institute, or they call it by its acronym, USAMRIID, drawling it as You Sam Rid. Or they call the place RIID, as in getting rid of something. Vent stacks on its roof discharge filtered exhaust air from sealed biological laboratories inside the building. Fort Detrick, the envelope of USAMRIID, sits in rolling country on the eastern slope of the Appalachian Mountains, in the drainage of the Potomac River. The Potomac bends through oak-blanketed mountains at Harpers Ferry and enters farmland, and eventually passes near Reston, Virginia, a town outside the Washington Beltway where farms give way to business parks, and where in the eighties office buildings accreted like crystals.

The mission of USAMRIID is medical defense. The Institute conducts research into ways to protect soldiers against biological weapons and natural infectious diseases. It specializes in vaccines, drug therapy, and biocontainment. That is, the Institute knows methods for stopping a monster virus before it ignites an explosive chain of lethal transmission in the human race. The laboratory suites at USAMRIID are maintained at four levels of biological security. The levels go from Biosafety Level 1, which is the lowest, up to Biosafety Level 4, the highest. The Biosafety Level 4 rooms contain BL-4 agents, also known as hot agents. A BL-4 hot agent is a lethal virus for which, in most cases, there is no vaccine and no cure. It is in the nature of hot agents to travel through the air: they can become airborne. The hot agents live in the hot suites in blood serum and bits of meat, frozen at -70° Centigrade. All the biocontainment laboratories at USAMRIID are kept under negative air pressure, so that if a leak develops air will flow into the hot rooms and out of the normal world, rather than the other way around. The Army does not publish a list of the viruses it keeps in the hot suites at USAMRIID, but here is a list of BL-4 viruses: Junin. Lassa. Machupo. Tick-borne encephalitis virus complex. Guanarito. Crimean-Congo. Marburg. Ebola Sudan. Ebola Zaire. Ebola Reston. If you want to shake hands with one of these viruses, you had better wear a space suit. That’s a federal rule. It holds equally at USAMRIID and at the Centers for Disease Control, in Atlanta, which are the only two laboratories in the United States that can handle BL-4 viruses.

To go inside a Biosafety Level 4 hot suite that contains life, first you have to strip naked. You put on surgical scrubs and then a space suit. You pull the helmet down over your head and close the suit. Then you enter an antechamber, a kind of air lock. It leads to Biosafety Level 4. Military people consider this air lock a gray zone, a place where two worlds meet. The air-lock doors are blazed with the international symbol for biohazard, a red trefoil that reminds me of a flower. I think it looks not unlike a red trillium, or toadshade. At USAMRIID, toadshades bloom in the gray zones.

Lieutenant Colonel Nancy Jaax is the chief of the pathology division of USAMRIID. She is a slender and rather beautiful woman, a doctor of veterinary medicine, forty-two years old, with curly auburn hair and green eyes. She has a brisk manner. On the job, Nancy Jaax wears a uniform consisting of green slacks and a green shirt with shoulder bars displaying the silver oak leaves of her rank. Or she wears a space suit. She is married to Colonel Gerald Jaax, who is the chief of the veterinary-medicine division at USAMRIID. The Army assigned Nancy Jaax and her husband to USAMRIID in 1979. She had just been awarded the rank of major, and she entered the pathology training program at USAMRIID as a veterinary-pathology resident. Pathologists at USAMRIID, who cut up hot tissue, are given vaccinations for lethal agents. Nancy Jaax said to me, “My vaccinations were for yellow fever, Q fever, Rift Valley—there were so many. The V.E.E., E.E.E., and W.E.E. complex, anthrax, and botulism. And, of course, rabies, since I’m a veterinarian.” She had an underlying medical condition that caused her immune system to react badly to the shots: the shots made her sick. The Army therefore stopped her vaccinations and assigned her to work in a space suit in the Biosafety Level 4 suites. “There aren’t any immunizations for most BL-4 agents, and that’s why you work in a space suit,” she explained.

In 1980, Nancy Jaax joined a group of military scientists who were performing experiments with Ebola virus on monkeys. They were infecting monkeys with Ebola and then treating them with interferon and other substances to see if the treatments stopped or weakened the disease. The purpose of the experiments was to find some chemical therapy for military personnel who might become infected with Ebola.

Ebola is one of a class of viruses known as the filoviruses. That means thread viruses. They look like spaghetti. As of this writing, the class comprises three subtypes of Ebola and a virus known as Marburg. Ebola virus is named for the Ebola River, a tributary of the Zaire (Congo) River which runs through northern Zaire. The first known emergence of Ebola Zaire—the hottest subtype of Ebola virus—happened in September, 1976, when the virus erupted simultaneously in fifty-five villages near the Ebola River. Ebola Zaire is a slate-wiper in humans. It killed eighty-eight per cent of the people it infected. Apart from rabies and the human immunodeficiency virus, H.I.V., which causes AIDS, this was the highest rate of mortality that has been recorded for a human virus. Ebola was spread mainly among family members, through contact with bodily fluids and blood. Many of the people in Africa who came down with Ebola had handled Ebola-infected cadavers. It seems that one of Ebola’s paths wends to the living from the dead.

Ebola victims died about a week after the onset of the first symptom, which was a headache. The Ebola patient soon breaks into a relentless fever, and then come the complications. Ebola triggers a paradoxical combination of blood clots and hemorrhages. The patient’s bloodstream throws clots, and the clots lodge everywhere, especially in the spleen, liver, and brain. This is called D.I.C., or disseminated intravascular coagulation. D.I.C. is a kind of stroke through the whole body. No one knows how Ebola triggers blood-clotting. As the strokelike condition progresses and capillaries in the internal organs become jammed with clots, the hemorrhaging begins: blood leaks out of the capillaries into the surrounding tissues. This blood refuses to coagulate. It is grossly hemolyzed, which means that its cells are broken. You are stuffed with clots, and yet you bleed like a hemophiliac who has been in a fistfight. Your skin develops bruises and goes pulpy, and tears easily, and becomes speckled with purple hemorrhages called petechiae, and erupts in a maculopapular rash that has been likened to tapioca pudding. Your intestines may fill up completely with blood. Your eyeballs may also fill with blood. Your eyelids bleed. You vomit a black fluid. You may suffer a hemispherical stroke, which paralyzes one whole side of the body and is invariably fatal in a case of Ebola. In the pre-agonal stage of the disease (the endgame), the patient leaks blood containing huge quantities of virus from the nose, mouth, anus, and eyes, and from rips in the skin. In the agonal stage, death comes from hemorrhage and shock.

People seem unable to develop protective antibodies to Ebola. You can’t fight off an Ebola infection the way you fight off a cold. Ebola seems to crush the immune system. The virus perhaps makes immunosuppressant proteins. No one knows the nature of such proteins, since there aren’t many virologists who care to study a virus for which there is no vaccine and no cure. (They don’t want the virus to do research on them.) Immunosuppressive proteins—if, indeed, they exist—would act as molecular bombs that ruin parts of the immune system, enabling the virus to multiply without opposition.

Like all viruses, Ebola and its cousin Marburg are parasites. They can copy themselves only inside a cell. Viruses need to use a cell’s equipment to reproduce. Ebola and Marburg grow promiscuously in human tissue, sprouting from cells like hair, forming tangled masses and braids and “g”s and “y”s and pigtails. Marburg-virus particles often roll up into tiny Cheerios. All filoviruses form semi-crystalline blocks inside cells, which are known as inclusion bodies. Some scientists call them bricks. The bricks may pack a cell until there’s almost nothing left of the cell but bricks: the cell bloats into a sack of bricks. Then the bricks break apart into threads of virus, and the threads push through the cell wall like grass rising from seeded loam.

A classic sign of infection by Ebola or Marburg is a certain expression that invariably creeps over the patient’s face as the infection progresses. The face becomes fixed and “expressionless,” “masklike,” “ghostlike” (in the words of doctors who have seen it), with wide, deadened, “sunken” eyes. The patient looks and sometimes behaves like a zombie. This happens because Ebola damages the brain in some way that isn’t known. The classic masklike facial expression appears in all primates infected with Ebola, both monkeys and human beings. They act as if they were already embalmed, even though they are not yet dead. The personality may change: the human patient becomes sullen, hostile, agitated, or develops acute psychosis. Some have been known to escape from the hospital.

Disseminated clotting cuts off the blood supply to tissues, causing focal necrosis—dead spots in the liver, spleen, brain, kidneys, and lungs. In severe cases, Ebola kills so much tissue that after death the cadaver rapidly deteriorates. In monkeys, and perhaps in people, a sort of melting occurs, and the corpse’s connective tissue, skin, and organs, already peppered with dead areas and heated with fever, begin to liquefy, and the slimes and uncoagulated blood that run from the cadaver are saturated with Ebola-virus particles. That may be one of Ebola’s strategies for success.

Lieutenant Colonel Nancy Jaax’s job during the Army’s 1980 experiments with Ebola was to dissect and examine monkeys that had died of the virus. Her space suit had triple pairs of gloves. First, there was an inner latex surgical glove. Over that, the suit had attached to it a heavy rubber glove. Over the rubber glove she wore another latex surgical glove. Her space suit and gloves were often splashed with blood as she cut into dead monkeys, and she regularly dipped her gloves in a pan of Envirochem—a liquid disinfectant that the Army believes is effective on viruses—to rinse away the blood. They use a buddy system in BL-4. You don’t work alone in a hot area. The buddies are trained to glance at each other’s gloves for leaks. (“The weak link is your glove,” Jaax told me. “You are handling needles, knives, and sharp pieces of bone.”) One day, Jaax’s buddy noticed a hole in Jaax’s right outer latex glove. The glove was covered with Ebola-laden blood. Jaax rinsed the glove in Envirochem and took it off, and found monkey blood inside it: the blood had run through the hole and drenched the heavy rubber glove.

Then she felt something clammy inside the heavy glove. She wondered if it was a leaker.

She rinsed her bloody glove and went into the air lock. There, still wearing her space suit, she pulled a chain to start the decontamination, or “decon,” cycle. The decon cycle took five minutes. First, a hot-water shower came on, and then came a mist of Envirochem, which washed away any blood from the exterior of her suit, while sterilizing it. She stepped into a tub of Envirochem, bent over, put her hands in the tub, and scrubbed her booties and gloves with a brush. (In the old days, the Army’s air-lock showers ran with Lysol. It kills germs, as advertised, but it made some people itch.) Then a final water shower came on and stopped. Nancy Jaax left the air lock and entered a staging area, where she stepped out of her space suit, withdrawing her latex-gloved hands from the suit’s heavy gloves. As her right hand came out of the suit, she saw it was red—bloody. The suit’s heavy glove had been a leaker.

The blood had smeared the innermost latex glove, right against her skin. Her heart pounded, and her stomach turned over. “I got that oogh feeling. That feeling you sometimes get when you work with these agents,” she said. “I went, ‘Oh, shit. What now? Oh, Jesus. What do I have to do now?’ ” On her right hand, under the last glove, she had an open cut in her skin. She does all the cooking for her family; she had cut herself with a paring knife while slicing vegetables, and had covered the cut with a Band-Aid. The question was whether any blood had penetrated the last glove to the Band-Aid and the cut. If so, it would amount to a death warrant. Five or ten virus particles suspended in a microscopic droplet of blood could easily slip through a pinhole in a surgical glove, and that would probably be enough to start a fatal infection. At USAMRIID, there is a group of pressurized hospital rooms designed so that patients can be treated by nurses and doctors wearing space suits. The place is an isolation hospital, and they call it the Slammer. Nancy Jaax began to wonder if she would end up in the Slammer by nightfall. She and her husband have two children. She did not want to break with Ebola virus in the Slammer and never see her children again. She dipped her last, bloody glove in Envirochem, and went over to a sink, and removed the glove. She put it under a faucet and filled it with water, like a water balloon. It held. No leaks. “This incident came into the category of close call,” she said to me.

Nancy Jaax continued with the experiment, and all the monkeys that had been infected with Ebola died; the drugs had no effect on the course of the disease. She kept two control monkeys—healthy monkeys—apart from the others, in separate cages inside the hot suite. Then both control monkeys died of Ebola. They had not been injected with virus, and their cages were on the far side of the room from those of the sick monkeys. “So the question is: How did they get it?” Lieutenant Colonel Nancy Jaax said to me. “They probably got it from aerosolized droplets from the sick monkeys. That was when I knew that Ebola could spread through the air.”

A virus is a small capsule consisting of membranes and proteins. The capsule holds one or more strands of RNA or DNA that contain the software program for making a copy of the virus. The virus penetrates a cell wall, and the capsule breaks apart inside the cell, releasing the strands of genetic material, which take over the cell and force it to make copies of the virus. Eventually, the cell gets pigged with virus, and pops. Or viruses can bud through a cell wall like sweat coming off a drip hose. In either case, viruses tend to kill cells. If they kill enough cells, or if they kill a class of cell that the host needs for survival, then the host dies. Viruses that kill their hosts do not themselves survive. It is in the virus’s best interest to let the host live, but accidents happen. Some biologists classify viruses as “life forms”—ambiguously alive. Bacteria and cells are always humming with activity, enzymatic processes. Viruses that are outside cells merely sit there; nothing happens. But when they get inside a cell they switch on and begin to replicate. Viruses can seem alive when they multiply, but in another sense they are molecular machines—obviously non-living, strictly mechanical, no more alive than a jackhammer. Compact, logical, hard, engineered by the forces of evolution, and totally selfish, the viral machinery is dedicated to making copies of itself—which it can do on occasion with radiant speed.

Viruses are not easy to see, even with an electron microscope. Here is a way to imagine the size of a virus. Consider the island of Manhattan, shrunk to this size:

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This shrunken Manhattan could easily hold nine million common-cold viruses. If you made an aerial reconnaissance of it with an electron microscope, you would see little figures milling like the lunch crowd on Fifth Avenue. Viruses can be purified and concentrated into crystals. Packed in a crystalline layer, shoulder to shoulder and only one virus deep, a hundred million polio viruses could cover the period at the end of this sentence. There could be a thousand Giants Stadiums of viruses sitting on that period—two hundred and fifty Woodstocks of viruses, a third of the population of the United States, sitting on that period—but you wouldn’t know it without a scope.

In 1892, a Russian scientist named Dimitry Ivanovsky studied a disease of tobacco leaves which gives them white spots. He passed the juice of sick leaves through extremely fine filters, and when he injected healthy plants with the filtered juice they got sick and developed white spots. Ivanovsky concluded that some very small agent was causing the disease, but he didn’t know whether it was a toxic chemical or a living thing. In 1898, Martinus Beijerinck, a Dutch botanist, proved that Ivanovsky’s virus was a replicative infectious agent. It has since come to be called tobacco-mosaic virus. In 1900, the United States Army discovered the first human virus—the yellow-fever agent. That was the work of Walter Reed and his team. The Army has tracked viruses from the beginning.

There is no fossil record in rocks to indicate that viruses existed before the late nineteenth century, when tobacco-mosaic virus was first noticed. Fossils of bacteria have turned up in rocks that are more than three billion years old, but no fossils of viruses have ever been found. Nevertheless, viruses are obviously ancient, and perhaps primeval. They are molecular sharks, a motive without a mind. They have sorted themselves into tribes, and they infect everything that lives.

The human immunodeficiency virus, or H.I.V., is a not very infectious but lethal Biosafety Level 2 or 3 agent, which most likely emerged from the rain forests of Central Africa. You don’t need to wear a space suit while handling blood infected with H.I.V. During the nineteen-seventies, the virus fell like a shadow over the human population living along the east-west highway that links Kinshasa, in Zaire, with Mombasa, in Kenya. The emergence was subtle: the virus incubates for years in a human host before it kills the host.

A zoonotic virus is a virus that lives naturally in an animal and can infect human cells, perhaps mutating slightly in the course of passage, which enables the virus to start a chain of infection through human hosts. For example, H.I.V.-2 (one of the two major strains of H.I.V.) may be a mutant zoonotic virus that jumped into us from an African monkey known as the sooty mangabey, perhaps when monkey-hunters touched bloody tissue. No one really knows where H.I.V. came from. H.I.V.-1 (the other strain) may have jumped into us from chimpanzees, or it may be a human virus that has been in our species for ages,circulating in some isolated group of people in Central Africa. As outsid-ers came into the area, AIDS came out, and passed into the general human population.

The emergence of AIDS appears to be a natural consequence of the ruin of the tropical biosphere. Unknown viruses are coming out of the equatorial wildernesses of the earth and discovering the human race. It seems to be happening as a result of the destruction of tropical habitats. You might call AIDS the revenge of the rain forest. AIDS is arguably the worst environmental disaster of the twentieth century, so far. Some of the people who worry in a professional capacity about viruses have begun to wonder whether H.I.V. isn’t the only rain-forest virus that will sweep the world. The human immunodeficiency virus looks like an example rather than a culminating disaster. As lethal viruses go, H.I.V. is by no means nature’s preëminent display of power. The rain forest, being by far the earth’s largest reservoir of both plant and animal species, is also its largest reservoir of viruses, since all living things carry viruses. Just how large the tropical reservoir of viruses is no one knows, but here is one way to consider the question. The earth is estimated to contain between three million and thirty million species of plants and animals. Most of the species are fungi, insects, and non-insect arthropods, such as ticks and mites, and the bulk of them live in tropical forests. Viruses often adapt to one or two species. For example, human beings carry more than a hundred different cold viruses that are adapted almost exclusively to the human host. If we suppose that every species carries one virus exclusively adapted to it, then there may be from three to thirty million strains of viruses. Possibly the number of virus strains is much larger than that—perhaps a hundred million—but nobody has ever tried to count them.

When an ecosystem suffers degradation, many species die out and a few survivor-species have population explosions. Viruses in a damaged ecosystem can come under extreme selective pressure. Viruses are adaptable: they react to change and can mutate fast, and they can jump among species of hosts. As people enter the forest and clear it, viruses come out, carried in their survivor-hosts—rodents, insects, soft ticks—and the viruses meet Homo sapiens. Here are the names of some emerging viruses: Lassa. Rift Valley. Oropouche. Rocio. Q fever. V.E.E. Guanarito. Ross River. Monkeypox. Dengue. Chikungunya. Hantaan. Machupo. Junin. The rabies-like strains Mokola and Duvenhage. Le Dantec. Human immunodeficiency virus—which might have been called Kinshasa Highway, if it had been noticed earlier—is considered an emerger, since its penetration of the human race is incomplete and is still happening explosively, with no end in sight. The Kyasanur Forestvirus. The Semliki virus. Crimean-Congo. Sindbis. O’nyong-nynong. Marburg. Ebola. Most of them—but not all—come from tropical forests or tropical savannas. When a virus that lives in some nonhuman host is about to crash into the human species, the warning sign may be a spatter of breaks—disconnected emergences, at different times and places. I tend to think of rats leaving a ship. The presence of international airports puts every virus on earth within a day’s flying time of the United States.

Reston, Virginia, is near Washington.The town has an active chamber of commerce and a visitors’ center designed to lure high-technology businesses to the area. Along the Leesburg Pike, a commuter route that funnels traffic to Washington, you see developments of executive homes. The homes are pseudo-Victorians, with unused porches, and stick-built neo-Georgians, with false-brick fronts and a Baby Benz parked in a semicircular carriageway. You also see the occasional bungalow with cardboard stuffed in a broken window and a Harley in the driveway. The town of Reston is bisected by the Dulles Access and Toll Road, which connects Dulles airport with Washington. Not far from the Dulles Access Road in Reston is a small business park. Until recently, a company called Hazleton Research Products had a monkey house in a one-story building in the business park. It was known as the Reston Primate Quarantine Unit. Hazleton Research Products sells animals for research; it is a division of Corning Incorporated. Hazleton was importing monkeys from the tropics and bringing them through J.F.K. International Airport to the Reston Primate Quarantine Unit. Each year, about sixteen thousand wild monkeys are imported into the United States, to be used as laboratory animals. Federal regulations require that imported monkeys be held in quarantine for at least thirty-one days before they are shipped anywhere else in the United States. This is to prevent the spread of infectious diseases that could kill other primates, including laboratory workers.

Dan Dalgard, doctor of veterinary medicine, is the principal scientist at Hazleton Washington, which has its offices on the Leesburg Pike, in Vienna, next to Reston. Dan Dalgard has an international reputation as a knowledgeable and skilled veterinarian who specializes in primate husbandry, and he understands monkey behavior and monkey diseases. He is a calm, blunt man in his late fifties. He wears glasses, and he has a square, pleasant face. On evenings and weekends, he repairs antique clocks as a hobby. He likes to use his hands and his mind to figure out how a broken complicated system can be fixed. Dalgard sometimes has longings to leave veterinary medicine and immerse himself in clocks.

On Wednesday, October 4, 1989, Hazleton accepted a shipment of a hundred wild monkeys from the Philippines. The shipment originated on the island of Mindanao, at a Philippine monkey-export company. The monkeys were macaques, and the species was Macaca fascicularis. Zookeepers call it the crab-eating macaque. It is a common monkey that lives along rivers and in mangrove swamps in Southeast Asia, and it is often used as a laboratory animal. It eats fruit, crabs, insects, and small pieces of clay. A crab-eating macaque will snatch a crab out of the water and quickly rip its claws off and throw them away before devouring the rest of the crab. Sometimes a crab-eating macaque isn’t quick enough with the claws, and when the monkeys are on a feeding bout in a mangrove swamp at low tide you can occasionally hear shrieks when a crab fastens on a monkey. The crab-eating macaque has brown eyes, pointed ears, tawny fur, and a long tail. As monkeys go, crab-eating macaques have a calm temperament, provided that you don’t stare at them. Any monkey thinks staring is rude, and the crab eater will respond on the same level, screaming “Kra, kra! ” and hurling its feces at you.

The Philippine monkeys arrived at J.F.K. and were taken by truck to Hazleton’s Reston Primate Quarantine Unit. The monkeys were kept in stainless-steel cages in windowless rooms, under artificial lights, and were fed monkey biscuits. The Reston quarantine rooms were designated by letters ofthe alphabet, from “A” through “L.” The Philippine monkeys were put in Room F. The ventilation system recirculated some air in common through the rooms, so that the monkeys were breathing one another’s air.

By the first of November, twenty-seven monkeys had died. That was more than usual for a shipment of wild monkeys. Dan Dalgard performed necropsies on the ones that had died, and concluded that they were being killed by dysentery and pneumonia. These diseases are not uncommon in wild monkeys. A week later, on Monday, November 6th, another shipment of crab-eating macaques arrived, making a total of about five hundred monkeys in the quarantine unit, all crab-eating macaques from the Philippines. But by November 10th Dalgard had begun to suspect that some of his monkeys might be dying of simian hemorrhagic fever, or S.H.F., a virus that is lethal to monkeys but does not cause clinical disease in humans. (It infects people but doesn’t make them sick.) The possibility worried Dalgard, because S.H.F. is highly contagious in monkeys, and can wipe out a colony.

He began sacrificing monkeys that appeared sick, by injecting them with overdoses of an anesthetic, and then he opened them up. He found that their spleens were enlarged—a classic sign of simian hemorrhagic fever. But monkeys infected with S.H.F. typically die sneezing blood or with other evidence of hemorrhaging, and Dalgard hadn’t seen any of these signs in the monkeys that died before November 10th. The monkeys had simply stopped eating and died of shock. The focus of the infection was Room F, where most of the monkeys had perished. The disease gave Dalgard an eerie feeling, and prompted him to keep a diary. Of the monkeys that had died in Room F he wrote:

Many of the animals were in prime condition and had more abdominal and subcutaneous fat than is customary for animals arriving from the wild. The diagnosis at this time was continuing to point more strongly toward S.H.F. but the slow progression [of the disease] and the lack of the hemorrhagic component confused the diagnosis.

He decided to take the mystery to the United States Army Medical Research Institute for Infectious Diseases, where he knew about a virologist named Peter Jahrling, who had done work on S.H.F. He described to Jahrling the illness that was burning through his monkeys, and he sent some blood and tissue samples to Jahrling. Some of the samples came from a monkey known as O53, which had lived in Room F. Jahrling froze some of the tissues and placed them in a Biosafety Level 3 containment room. This level is kept under negative pressure, but you don’t need to wear a space suit inside it.

One way to identify a virus is to make it multiply inside living cells in a flask. You drop a very small sample of the virus into the cells, and as the virus spreads through the cells extraordinary numbers of virus particles are produced. You can then look at them under a microscope, or you can put different kinds of fluorescent antibodies—immunity proteins—in the virus culture. These antibodies attach themselves to infected cells and glow under ultraviolet light, and the antibody that makes cells glow tells you which particular virus you have in the flask.

A civilian technician named Joan Rhoderick cultured the unknown monkey virus from the liver of Monkey O53. She ground up a bit of the liver with a mortar and pestle, and dropped some of the resultant mush into flasks that contained a living strain of cells from the kidney of a green monkey. Joan Rhoderick wore a surgical mask and rubber gloves but not a space suit, and she worked with the samples kept in a safety cabinet that pulls air away from the samples and through a filter.

John Rhoderick and Peter Jahrling looked at slices of liver and spleen from Monkey O53, and Jahrling gave a presumptive diagnosis of simian hemorrhagic fever to Dan Dalgard. At this point, Dalgard felt that he had no choice but to sacrifice all the monkeys in Room F in order to halt the spreading disease. If those monkeys were infected with S.H.F., they would die anyway, and if they weren’t sacrificed the disease could spread to other rooms, killing more monkeys. Dalgard and an assistant, wearing surgical masks and rubber gloves, euthanized all the monkeys in Room F on November 16th—some seventy monkeys in all. They gave the monkeys injections of an anesthetic. Dalgard opened ten of the corpses to see what he could see, and sent everything to an incinerator.

At the beginning of Thanksgiving week of 1989, when these events were taking place at the Reston Primate Quarantine Unit, Thomas Geisbert was a twenty-seven-year-old civilian researcher working at USAMRIID while he studied for a Ph.D. in microbiology. His specialty is the electron microscope. Geisbert is something of a loner, a tall man with blue eyes, brown hair, and arrestingly large ears. He grew up an only child in western Maryland, where he spent a lot of time camping in the woods alone or with his uncles, who taught him how to hunt and fish. Geisbert’s boss at USAMRIID was Peter Jahrling. Tom Geisbert goes deer hunting in West Virginia every year around Thanksgiving. He planned to leave on Monday morning of that week, but something prompted him to stop by his lab at USAMRIID for a last look at the flasks of monkey cells that were incubating the virus from Reston. At nine in the morning, he put on a surgical mask and gloves and entered the BL-3 suite. There he met Joan Rhoderick, the technician who had started the Reston culture. She was looking at a flask under a microscope. The flask contained cells infected with virus from the Reston monkey O53. She said to Geisbert, “There’s something flaky going on in this flask.”

The flask was small—four inches long—and it was made of plastic and had a screw cap. Geisbert looked through the eyepieces of the microscope into the flask. Living cells ordinarily cling to the bottom of a flask in a carpet. This carpet looked eaten by moths. It was full of holes: dead and dying cells had detached from the flask and drifted into the fluid. Later, he described to me what he’d seen. “Cells that have been infected with S.H.F. take on a spiderweb look. These cells didn’t look like that. They were rounded and had a granular, pepperlike look. Some were dead. They were ‘off the plastic,’ as we say. It means they had floated away.”

This didn’t look like simian hemorrhagic fever. He went out and got Peter Jahrling, his boss. He said to Jahrling, “There’s something very strange going on in that flask, but I’m not sure what.”

Jahrling had worked at USAMRIID long enough to have seen some strange things in flasks. “The cells were blown away. They were crud,” Jahrling recalled later. He thought that a wild strain of bacteria had invaded the cell culture. This is a common and annoying occurrence in cell cultures, and it wipes out the culture. Bacteria give off odors as they multiply, and Peter Jahrling had smelled enough bacterial contaminations so that he knew how to distinguish them by nose. Viruses, on the other hand, kill cells without releasing an odor. Jahrling guessed that the flask had been wiped out by a common soil bacterium named pseudomonas, which, he says, “smells like Welch’s grape juice.” He unscrewed the cap and waved his hand over it, and took a whiff, and said to Geisbert, “Have you ever smelled pseudomonas?” Geisbert accepted the flask from Jahrling and sniffed. He didn’t smell any Welch’s grape juice. There was no odor. Jahrling, who hadn’t smelled anything, either, took back the flask and whiffed it again. Nothing. No smell. But the cells were blown away.

Geisbert poured some milky fluid out of the flask into a test tube and spun it in a microcentrifuge. A small “button” of material collected at the bottom of the test tube—a pill of dead and dying cells. Geisbert removed the button with a wooden stick and soaked it in plastic resin. Then he went hunting in West Virginia. He planned to look at the button in his microscope when he returned, after Thanksgiving. When Ebola virus infects a human being, the incubation period is from seven to fourteen days, while the number of virus particles gradually climbs in the bloodstream. Then comes the headache.

The first known emergence of a filovirus happened in August, 1967, in Marburg, Germany. A shipment of green monkeys from Uganda had arrived in Frankfurt. Green-monkey kidney cells are useful for the production of vaccines, and these monkeys were going to be killed for their kidneys. Most of the monkeys were trucked from Frankfurt to a factory in Marburg that produced serum and vaccines, while a few monkeys from the same shipment stayed in Frankfurt, and a few others went to Belgrade, Yugoslavia. The first person known to be infected with the virus—the index case—was a man known as Klaus F., an animal-care technician at the serum factory in Marburg. He broke with fever and rash on August 8th, and died two weeks later.

So little is known about the Marburg agent that only one book has been published about it, “Marburg Virus Disease,” edited by G. A. Martini and R. Siegert. In it we learn:

The monkey-keeper heinrich p. came back from his holiday on August 13th 1967 and did his job of killing monkeys from August 14th-23rd. The first symptoms appeared on August 21st.

The laboratory assistant renate l. broke a test-tube that was to be sterilized, which had contained infected material, on August 28th, and fell ill on September 4th 1967.

And so on. Thirty-one laboratory workers acquired the disease; seven died. In other words, the case-fatality rate of Marburg virus in hospitalized patients was twenty-two per cent. That was terrifying. Yellow fever, which is considered a lethal virus, kills only five per cent of the infected once they reach a hospital.

Marburg began with a splitting headache, focussed behind the eyes and temples. That was followed by a fever. The characteristic diagnostic sign was a red speckled rash over the body which blistered into a sea of tiny white bubbles. “Most of the patients showed a sullen, slightly aggressive, or negativistic behavior,” Martini wrote. “Two patients [had] a feeling as if they were lying on crumbs.” One became deranged and psychotic. These mental signs were caused by the virus’s having damaged the brain. The patient Hans O.-V. showed no signs of mental change, but he suffered a sudden, acute fall of blood pressure and died. At autopsy, his brain was found to be laced with hemorrhages, and there was a massive, fatal hemorrhage at the center. In Frankfurt, an animal attendant known as B. developed a high fever and eventually began bleeding from his mouth, nose, and gastrointestinal tract. He was given whole-blood transfusions, but then he developed uncontrollable hemorrhages at the sites of the I.V. punctures. He died with blood running from his mouth and his nipples. All the survivors lost their hair. During convalescence, the skin peeled off their faces, hands, feet, and genitals. It was a small, frightening emergence.

Marburg virus looks like rope, or it rolls up into the rings that resemble Cheerios. Virologists had never seen a ring-shaped virus, and couldn’t figure out how to classify it. They thought that it might be a type of rabies. The rabies particle is shaped like a bullet, and if you stretch a bullet it becomes a rod, and the rod can be bent into a doughnut: Marburg. They started calling Marburg “stretched rabies.” But it is not related to rabies.

The question was: What is the virus’s natural history? In what animal or insect does Marburg hide? Marburg evidently does not circulate in monkeys. Monkeys die quickly of the disease, and if they were the reservoir, Marburg wouldn’t wipe them out. The monkey’s immune system would have learned to attack the virus, and the virus itself would have become better adapted to living in monkeys without killing them, since it is in the virus’s best interest to let the host survive. The Marburg monkeys had been collected in Uganda by native trappers—apparently in forested habitat to the west of Mt. Elgon, an extinct volcano that straddles the border between Uganda and Kenya. Teams of epidemiologists combed Uganda, and especially the western slopes of Mt. Elgon, looking for some animal or insect that harbored Marburg virus; they found nothing.

In 1980, a French engineer who was employed by the Nzoia Sugar Company at a factory in Kenya within sight of Mt. Elgon developed Marburg and died. He was an amateur naturalist who spent time camping and hiking around Mt. Elgon, and he had recently visited a cavern on the Kenyan side of the mountain which was known as Kitum Cave. It wasn’t clear where the Frenchman had picked up the virus, whether at the sugar factory or outdoors. Then, in the late summer of 1987, a Danish boy whose name will be given here as Peter Cardinal visited the Kenyan side of Mt. Elgon with his parents—the Cardinals were tourists—and the boy broke with Marburg and died.

Epidemiologists at USAMRIID became interested in the cases, and they traced the movements of the French engineer and the Danish boy in the days before their illnesses and deaths. The result was weird. The paths of the French engineer and the Danish boy had crossed only once—in Kitum Cave. Peter Cardinal had gone inside Kitum Cave. As for the Ugandan trappers who had collected the original Marburg monkeys, they might have poached them from the Kenyan side of Mt. Elgon. Those monkeys might have lived near Kitum Cave, and might even have occasionally visited the cave.

Mt. Elgon is a huge, eroded volcanic massif, fifty miles across—one of the largest volcanoes in East Africa. Kitum Cave is one of a number of caverns that penetrate Mt. Elgon at an altitude of around eight thousand feet and open their mouths in a deep forest of podo trees, African junipers, African olives, and camphors. Kitum Cave descends into tight passages and underground pools that extend an unknown distance back into Mt. Elgon. The volcanic rock within Kitum Cave is permeated with mineral salts. Elephants go inside the cave to root out chunks of salty rock with their tusks and chew on them. Water buffalo also visit the cave to lick the rocks, and they may be followed into the cave by leopards. Fruit bats and insect-eating bats roost in the cave, filling the air with a sour smell. The animals drop their dung in the cave—an enclosed airspace—and they attract biting flies and carry ticks and mites. The volcanic rock contains petrified logs, the remains of trees that were enveloped in lava, and the logs are filled with sharp crystals. Peter Cardinal may have handled crystals inside the cave and scratched his hands. Possibly the crystals were tainted with animal urine or the remains of an insect. The Army keeps some of Peter Cardinal’s tissues frozen in cryovials, and the Cardinal strain is viciously hot. It kills guinea pigs like flies. In February, 1988, a few months after Peter Cardinal died, the Army sent a team of epidemiologists to Kitum Cave.

The team wore Racal suits inside the cave. A Racal is a lightweight pressurized suit with a filtered air supply, used for hot operations in the field. There is no vaccine for Marburg, and the Army people had come to believe that the virus could be spread through the air. Near and inside the cave they set out, in cages, guinea pigs and primates—baboons, green monkeys, and Sykes’ monkeys—and they surrounded the cages with electrified wire to discourage predators. The guinea pigs and monkeys were sentinel animals, like canaries in a coal mine: they were placed there in the theory or the hope that some of them would develop Marburg. With the help of Kenyan naturalists, the Army team trapped as many different kinds of wild mammals as they could find, including rodents, rock hyraxes, and bats, and drew blood from them. They collected insects. Some local people, the il-Kony, had lived in some of the caves. A Kenyan doctor from the Kenya Medical Research Institute, in Nairobi, drew blood from these people and took their medical histories. At the far end of Kitum Cave, where it disappears in pools of water, the Army team found a population of sand flies. They mashed some flies and tested them for Marburg.

The expedition was a dry hole. The sentinel animals remained healthy, and the blood and tissue samples from the mammals, insects, arthropods, and local people showed no obvious signs of Marburg. To this day, the natural reservoir of Marburg is unknown. Marburg lives somewhere in the shadow of Mt. Elgon.

On July 6, 1976, five hundred miles northwest of Mt. Elgon, in the township of Nzara, Sudan, in densely wooded country at the edge of the African rain forest, a man referred to as YuG died of a hemorrhagic fever. He was a storekeeper in a cotton factory, and he was the index case of a new strain of filovirus. The clinical features of the disease were indistinguishable from those of Marburg—masklike facial expression, rash, bleeding, terminal shock. Two of YuG’s co-workers also came down with the disease and died. No one knows how the virus got into the cotton factory. One of the dead men, a man known as PG, had a wide circle of friends and contacts, and he also had several mistresses. Most of the subsequent fatal cases of what later came to be known as the Sudan subtype of Ebola hemorrhagic fever can be traced back through chains of infection to PG, through as many as six generations of infection. The strain burned through the town of Nzara, and then reached eastward to the town of Maridi, where there was a large hospital, and it hit the hospital like a bomb. It killed nurses and aides, and it savaged patients and then radiated outward from the hospital through patients’ families. (A characteristic of a lethal, highly transmissible, and incurable virus is that it kills medical people first. Frequently, as in this case, the medical-care system actually intensifies the outbreak, like a lens that focusses sunlight in a heap of tinder.) The Sudan virus was more than twice as lethal as Marburg—its case-fatality rate was fifty per cent, the same as that of bubonic plague before antibiotics. And the death rate kept climbing, until by the third month of the Sudan outbreak mortality among the infected had hit seventy per cent, as if perhaps the virus were mutating, getting hotter as it passed from generation to generation in humans. Then, for reasons that aren’t clear, the outbreak subsided. The surviving staff of the Maridi hospital had panicked and run away, and that may have helped break the chain of infection. Or possibly the human hosts died too quickly to be efficient transmitters of the virus. Whatever the reason, the organism vanished.

In early September, 1976, two months after the beginning of the Sudan break, a similar yet more lethal strain emerged five hundred miles to the west, in the Bumba Zone of Zaire, an area of humid rain forest drained by the Ebola River. The Ebola River strain seemed to come out of nowhere, and popped up in the Yambuku Mission Hospital, an upcountry clinic run by Belgian nuns. The nuns and staff at Yambuku were using five needles a day to give injections of antibiotics and vitamins to hundreds of people in the hospital’s outpatient and maternity clinics. The staff sometimes rinsed the needles in a pan of warm water between injections. The virus entered the cycle of dirty needles, and erupted in fifty-five villages around the hospital. It first killed people who had received injections, and then killed family members—particularly women, who in Africa prepare the dead for burial.

The virus also wiped out the Yambuku hospital’s medical staff. (Medical people go first.) By the end of September, two-thirds of the staff were dead or dying, and the hospital closed down. A critically ill Belgian nun who was a nurse at the hospital, Sister M.E., was flown to Kinshasa, the capital of Zaire, with another nun, Sister E.R., who nursed her. Sister M.E. was admitted to the Ngaliema Hospital, and she died there shortly afterward. Sister E.R. then became ill and died. Then a Zairian nurse at Ngaliema Hospital, identified as M.N., developed fever and bleeding. She had cared for Sister M.E.; she herself would soon die. While M.N. was incubating the virus, she had had face-to-face contact with several dozen people in the city of Kinshasa. The virus seemed about to start an explosive chain of lethal transmission in Kinshasa, a poor, crowded city with a population of two million, where the virus might go off like a bonfire. This epidemiological possibility triggered a panic in European capitals. Kinshasa has direct air links to Europe, and European governments contemplated blocking flights from Kinshasa. The World Health Organization feared that the nurse M.N. might be the vector for a worldwide pandemic. The Zairian government ordered its army to seal off the Bumba Zone with roadblocks, and all radio contact with the province was lost. Bumba had dropped off the earth, into the silent heart of darkness.

Out of Bumba came some tubes of blood, and from Sudan came some vials of serum. A few of the samples ended up in Atlanta, Georgia, at the Centers for Disease Control, where a team headed by Karl M. Johnson isolated the Ebola River virus for the first time. Key members of the team were Frederick A. Murphy, who is an expert in the electron microscope, and Patricia A. Webb, a virologist. (She was married to Karl Johnson at the time.) The team started to grow the virus in cultures of monkey cells, and Murphy began looking at the cells in his microscope. On October 13th, Webb telephoned her husband, Johnson, and said to him, “Karl, you’d better come quick to the lab. Fred has harvested some cells, and they’ve got worms.” The virus looked like Marburg, but Johnson found that it didn’t react to Marburg antibodies. Therefore it was a new virus. Karl Johnson and his team had performed what is known as the first isolation and characterization of the agent—they had got it to replicate, and they had proved it was something new. (Teams at the Microbiological Research Establishment in Porton Down, England, and at the Institute for Tropical Medicine in Antwerp, Belgium, had isolated the virus, too, but they didn’t know what it was.) Johnson’s team had earned the right to name the organism. They named it Ebola.

I learned that Johnson could be reached at a fax number in Big Sky, Montana, so I sent him a fax, in which I said that Ebola virus fascinated me. My fax machine emitted this reply:

Mr. Preston:

Unless you include the feeling generated by gazing into the eyes of a waving confrontational cobra, “fascination” is not what I feel about Ebola. How about shit scared?

The richest trout river in America may be the Bighorn, a green, muscular river in Montana that flows out of the Bighorn Mountains into grassland, and is lined with cottonwoods. One recent day in October, the brown trout were spawning in the Bighorn, and the cottonwoods had turned yellow and rattled in a south wind. Standing waist-deep in a mutableslick of the river, wearing sunglasses, with a cigarette hanging from the corner of his mouth and a fly rod in his hand, Karl Johnson ripped his line off the water and laid a cast upstream. Johnson is a great figure in the history of virology; he trained an entire generation of field virologists at a tropical laboratory called MARU, which he ran in Panama. “I’m so glad nature is not benign,” he said. He studied the water, took a step downstream, and whipped another cast. “But on a day like today, we can pretend nature is benign—all monsters and beasts have their benign moments.” Johnson was a member of a World Health Organization team that went to Kinshasa to try to contain the Ebola virus. “When we got to Kinshasa, the place was an absolute madhouse. There was no news coming out of Bumba province, no radiocontact. We knew it was bad in there, and we knew we were dealing with something new. We didn’t know if the virus could be spread by droplets in the air, somewhat like influenza. If Ebola had easily spread through the air, the world would be a very different place today.”

“How so?”

“There would be a lot fewer of us. It would have been exceedingly difficult to contain that virus if it had had any major respiratory component.”

“Were you afraid you wouldn’t come out alive?”

“Yeah. But I’d been there before. In 1963, I led the investigation of the Machupo outbreak, named for a river that runs by a little town in the plains of eastern Bolivia. Same kind of thing. People bleeding and dying.”

Karl Johnson performed the first isolation of the Machupo virus, a deadly emerger that belongs to a family known as the arenaviruses, because the virus particles are speckled with dots that look like sand. (Arena is Latin for “sand.”) Johnson came down with Machupo in Bolivia—he went into borderline shock in a hospital in the Canal Zone, after he’d been flown out of Bolivia, and he nearly died. Johnson also collaborated on the first isolation of the Hantaan virus, a lethal east-Asian organism (classified as a BL-3 agent), which happens to be another important emerger. A Hantaan relative now infects the rats of Baltimore and Philadelphia; no obvious human epidemic has yet occurred in the United States. Johnson has therefore been credited with work that led to the discovery and classification of three major groups of emerging human hemorrhagic-fever viruses—the filoviruses, the arenaviruses, and the hantaviruses (named after Hantaan).

“I’ve seen young physicians run from these hemorrhagic viruses, literally,” he said. “In the Zaire thing, we had a young doctor from the C.D.C. who just couldn’t get on the plane with me to Kinshasa. He admitted he was too afraid. We sent him home. I did figure that if Ebola was the Andromeda strain—incredibly lethal and spread by droplet infection—then there wasn’t going to be any safe place in the world anyway. It was better to be working at the epicenter than to get the infection at the London opera.”

The W.H.O. team in Zaire wore fabric helmets with full-face respirators, and disposable gowns, gloves, and overshoes. They set up two containment pavilions at Ngaliema Hospital. Into one pavilion they shut thirty-seven people who had had face-to-face contact with M.N., the Zairian nurse who was then dying, and into the other pavilion they shut all medical staff who had had contact with the nuns who had already died. Doctors and nurses entered the containment areas through a double-doored antechamber, a gray zone. They wrapped the cadavers of the nuns and the nurse (when she died) in sheets soaked in a phenolic disinfectant, then double-bagged these mummies in plastic, put them in coffins that had screw-down lids, and issued instructions to the families of the deceased to bury the coffins immediately, with no wake. The rooms where the nuns had suffered their agonals were not pleasant to behold. The floors, furniture, and walls were stained with blood. The aspect of those rooms may have raised in some minds one or two questions about the nature of the Supreme Being; or, for persons not inclined to theology, the blood on the walls may have served as a reminder of the nature of Nature. The team washed everything with bleach and smoked the victims’ rooms with formaldehyde vapor. No one in the containment pavilions or in the city fell ill with the virus. Somewhat to the team’s surprise, and to its great relief, the Ebola agent seemed not to be contagious in face-to-face contacts.

“We got an advance party into the bush with a couple of Land Rovers,” Johnson said. “They wore respirators and paper gowns and rubber gloves. It turned out that the epidemic was already in decline when the teams got there. The village elders had had the wisdom to institute procedures for dealing with smallpox, which has been a problem for centuries in Africa. An infected person was put in a hut by himself, and food and water were pushed through the doorway. If the person was able to care for himself, he’d eventually come out of the hut. Otherwise, they’d burn the hut down. It really worked with Ebola. But think what that does to a traditional culture. In order to stop an epidemic that way, you have to suspend all the normal cultural relations that surround death. You have to put a parent or a child into that hut and burn it down afterward. The African technique would work in the United States, but I don’t think we’d do it.”

During Thanksgiving week of 1989, Nancy Jaax’s father was dying of cancer in Wichita, Kansas, and she and Jerry drove home. Nancy had grown up on a farm in Wichita. Her father had owned a small chain of hamburger restaurants called Dunn’s Grills. They lived on a farm outside town, where they grew truck crops, such as tomatoes, cantaloupes, peppers, watermelons, and corn, for the restaurants. Nancy would get up at five in the morning to work in the fields with her father. Later, in high school, she moved in with her grandmother in Wichita, and in the evenings she would help run another restaurant owned by her father called the Plantation (her father had sold Dunn’s Grills). Thanksgiving of 1989 was the most painful family reunion of her life. She said her farewell to her father. She didn’t know whether she would see him again.

Tom Geisbert shot a buck in West Virginia, and returned home to spend Thanksgiving with his family. Dan Dalgard spent an uneasy Thanksgiving with his wife. He had not stopped the apparent course of simian hemorrhagic fever in his monkeys by sacrificing the monkeys in Room F. Dead monkeys appeared in Room H, two doors down the hall from Room F. After the holiday weekend, Dalgard performed necropsies on four monkeys, taking slices of spleen, liver, and kidney. He wrote in his diary, “Gut feeling after looking at the animals and tissues is that we are not seeing lesions compatible with S.H.F.” He had no idea what was killing his monkeys.

At seven-thirty on Monday morning, November 27th, Tom Geisbert reported to work at his laboratory at USAMRIID. He wanted to get an early start with his electron microscope, looking at the button of dead cells he had harvested the previous Monday. Recently, I met with Geisbert in his office. The walls were plastered with photographs of the Ebola virus. Some of the viruses were ten inches long and resembled ballpark frankfurters. I asked him how he takes a photograph of a virus. He unlocked a filing cabinet and removed from it a metal object the size of a pocket pencil sharpener. “This is a diamond knife,” he said. “These things cost about four grand apiece. See the diamond?” Hesitantly, he slid his treasure across his desk toward me, and I picked it up. A prism gleamed. “Please don’t touch the edge,” he said. “You’ll completely trash it. You’ll dull it, and your finger oils will stick to the edge. Four thousand dollars.”

He showed me a button of cells. It was a dot the size of a toast crumb, embedded in a wedge of clear plastic. The cells—from a monkey’s liver—were almost rotten with Ebola virus, but he’d sterilized the button with chemicals. He took the button into another room, where he mounted the button and the diamond knife in a machine and threw a switch. The machine worked like a deli slicer. It drew the diamond knife across the button, peeling off a slice, just like a slice of luncheon meat. The slice was this size:

•

It contained as many as ten thousand cells. Geisbert picked up the slice with a tiny copper mesh, and carried the sample into a darkened room containing a metal tower taller than a person. That was his microscope. He put the sample in a chamber in the microscope, and pushed a button. A complicated image appeared on a viewing screen, showing a tiny corner of one cell—a cellscape of oxbow rivers and lakes that reminded me of an aerial view of jungle.

“I don’t see any Ebola here,” Geisbert declared, turning a knob, while the cellscape drifted across the field of view. We huddled over the viewing screen, and lakes and paths and specks went by almost without end, until I felt as if we were inside a starship, making a low-orbit pass over a huge, unexplored planet near Tau Ceti. “Sometimes the viruses are everywhere, or sometimes I have to look for six hours before I find a particle,” Geisbert said. He was immutably patient, his eyes scanning the terrain. He could pick out patterns of sickness in a cell, subtle anomalies which, like footprints, would lead him to the horrible brood. In the case of Ebola, it is a brood. When Ebola replicates, the virus grows in blocks inside a cell, which are like nests. These are the inclusion bodies, or bricks. The bricks migrate toward the surface of the cell. As a brick reaches the cell wall, it disintegrates into hundreds of individual viruses, and the broodlings bud through the cell membrane and float away in the universe of the host. No one knows how the Ebola bricks are propelled toward the surface of the cell.

“That was quite a day,” Geisbert said, sitting at the microscope in the darkened room. His face glowed in the light of the screen. “It’s in the morning, around ten o’clock. The sample is cell culture from Monkey O53. I put the sample in the scope. I switch it on. I’ve looked at it for maybe fifteen seconds, and then—‘Oh, shit.’ The tissue was a mess, and it was wall-to-wall with filovirus.” Some areas were so thick with virus that they looked like buckets of rope. “I almost lost it,” he said. “The only filovirus I’d ever seen in the microscope was Marburg. I had worked with the Cardinal strain of Marburg—the strain from the Danish boy who got Marburg at Kitum Cave in Mt. Elgon—and I knew what that looked like. So I thought, Marburg. I knew that Pete Jahrling and I had sniffed those flasks. I thought, Oh, man, Pete and I have been handling this stuff in BL-3 conditions, and this is a BL-4 agent.”

He developed a few photographs of the virus particles and hurried into the office of Peter Jahrling, his boss. Jahrling reacted calmly. It seemed to be a filovirus—Jahrling could see wormlike shapes. Jahrling and Geisbert could have breathed it into their lungs. They began counting days back to the time of their exposure. Seven days had passed since they inhaled from the flask. Well, they didn’t have headaches yet.

Jahrling went to get his boss, Colonel Clarence James Peters—he goes by the name C.J.—who was then the chief of the disease-assessment division at USAMRIID. Colonel Peters came into Jahrling’s office and looked at Geisbert’s photographs. Peters feared that any public announcement of a Marburg-virus outbreak might cause a panic in Reston, once people had learned the history of Marburg. He wanted to get a definite positive identification of the strain before the Army made any announcement.

Tom Geisbert stayed up most of that night. He went into the BL-3 laboratory and found a plastic jug that contained sterilized pieces of liver from Monkey O53. He fished some liver out of the jug, clipped bits off it, and fixed the bits in plastic, preparatory to slicing them for viewing in his electron microscope. He left the plastic to cure and went home for a couple of hours to try to sleep. He returned to Fort Detrick while it was still dark, at five in the morning, and before the sun rose he had developed photographs of filovirus particles budding directly out of cells in the monkey’s liver. It was a definite confirmation that the Reston monkeys were infected with a filovirus. But what strain was it? Everyone assumed that it was Marburg, which kills about one in four people it infects. All that day, in his laboratory, Peter Jahrling used a fluorescence test to try to nail down the strain. At five o’clock in the evening, he put some samples under an ultraviolet light and, to his shock, found that the stuff that glowed wasn’t Marburg: it was Ebola, the slate-wiper, which kills almost nine out of ten people.

The news that Ebola virus had broken out near Washington, D.C., was not received casually at Fort Detrick. Shortly after five o’clock, minutes after Jahrling typed the strain, Colonel Peters notified the chain of command. First, Peters and Jahrling went to Colonel David Huxsoll, the head of USAMRIID. Picking up Huxsoll and then Nancy Jaax, the group then went to Major General Philip Russell, the commander of the Army Medical Research & Development Command at Fort Detrick. General Russell was himself a virologist, and when he saw Geisbert’s glossy photographs he knew what he was looking at. The meeting became tumultuous. With people talking loudly in the background, General Russell picked up the telephone and called the Centers for Disease Control, and got Frederick Murphy on the line. Murphy is an expert on the Ebola virus—he had performed the first isolation of the virus with Karl Johnson, during the 1976 Zaire outbreak—and now, perhaps understandably, Murphy was skeptical when General Russell told him that the Army had isolated Ebola near Washington. Murphy is reported to have said to General Russell, “You can’t fool me. You have crud in your scope.” Still, Murphy took it seriously. He said that a team from the C.D.C. would fly to USAMRIID early the next morning to review the data. He advised Russell to notify Hazleton Research Products, so that the company’s employees could be protected, and also to notify the Virginia State Department of Health.

Russell and Huxsoll put C.J. Peters in charge of any Army units that would be needed to deal with the Ebola outbreak. Next, Peters set up a conference call with Dan Dalgard, at his home. He told Dalgard that his monkeys had Ebola virus, probably in a mixed infection with simian hemorrhagic fever. Dalgard had heard of Marburg but never of Ebola.

The next morning—Wednesday, November 29th—seven dead monkeys turned up in Room H at the Reston Primate Quarantine Unit. It seemed that Room H had now become the hot spot.

Then Dalgard got another disturbing piece of news. An animal caretaker at the Reston monkey unit, who will here be called Jarvis Purdy, had suffered a heart attack and had been taken to Loudoun Hospital, near Reston. Dalgard wondered if Purdy’s heart attack had been triggered by an Ebola infection. Had Purdy thrown an Ebola clot? Dalgard called the hospital and, without mentioning the word “Ebola,” left instructions for Purdy’s doctor that if he saw any unusual signs in Purdy he should immediately notify Colonel C. J. Peters, of the United States Army. Dalgard also issued an order to the monkey caretakers at the Reston unit. As he recorded in his journal,

All operations other than feeding, observation and cleaning were to be suspended. Anyone entering the rooms was to have full protection—Tyvek suit, respirator, and gloves. Dead animals were to be double-bagged and placed in a refrigerator.

That morning, Colonel Peters and Lieutenant Colonel Nancy Jaax drove down to Hazleton Washington’s headquarters, in Vienna, where Dalgard has his office and the company has a laboratory. Peters, in command of the Army groups that would respond to the Reston emergence in whatever way might be needed, sensed that the Army might have to act decisively to deal with the virus. As he drove to Vienna, he turned over in his mind the question of whether the Army would have to sterilize the Reston Primate Quarantine Unit, using military biohazard teams. There is a slang term in the Army for this type of action: the term is “nuke.” In the world of biocontainment, nuke has nothing to do with nuclear weapons. It has to do with neutralizing hot organisms: to nuke a place means to sterilize it. You go into the place in space suits and you isolate any infected hosts. If the hosts are animals, you kill them, bag them, and incinerate them. If the hosts are human, you put them in bubble stretchers and take them to the biocontainment hospital at USAMRIID—the Slammer. Then you sterilize the hot zone with biocides and formaldehyde gas.

C.J. Peters is not a hardboiled military type. He is a medical doctor and a field virologist of the old school, a jungle hand who got his training with Karl Johnson in Panama and worked with him during the Machupo outbreak in Bolivia. Peters has recently left the Army to become the chief of the Special Pathogens Branch of the Centers for Disease Control—a job that he landed at least partly because of the way he handled the Reston emergence. Peters is a chunky, affable man in his fifties, with a mustache, a round face, and what I think of as stingingly alert eyes.

Not wanting to attract attention, Peters and Lieutenant Colonel Jaax drove in separate civilian cars to the corporate office of Hazleton Washington. They were in uniform. At Hazleton, they talked with Dalgard and looked at slides of monkey tissue. They wanted to get samples, and perhaps some cadavers, and they wanted to see the monkeys at the monkey house face-to-face. Dalgard, perhaps fearful of losing control of the situation, would not allow them to visit the Reston Primate Quarantine Unit. Instead, the two Army officers drove four miles down the Leesburg Pike into Reston and parked in a cul-de-sac beside an Amoco station, near some pay telephones, waiting for someone from the Reston monkey house to bring them samples of monkey tissue. It was early afternoon. “We watched guys buying Cokes to drink, and housewives calling their boyfriends,” Peters said to me. Eventually a windowless Hazleton van pulled up and parked beside the colonels, and a Hazleton employee swung heavily out of the driver’s seat. “I’ve got ’em right back here,” he said. He threw open the door of the van, and the colonels saw seven garbage bags.

“I said to myself, ‘What is this?’ ” Peters recalled. The garbage bags held seven dead monkeys, and they were as hot as hell. Presumably lethal. They were the seven crab-eating macaques that had turned up dead that morning in Room H.

Jaax was getting that oogh feeling in the pit of her stomach. She turned to Peters. “I’m not putting that shit in the trunk of this car,” she said. “As a veterinarian, I have certain responsibilities with regard to transportation of dead animals, sir. I can’t just knowingly ship a dead animal with an infectious disease across state lines. You’re a doc. You can get away with this.” She nodded at his shoulder bars and said, “This is why you put on those big eagles, sir.”

Nancy Jaax wanted to dissect the monkeys as soon as possible, since she had noticed how Ebola-infected cadavers degenerate. (“If the animal has been dead for more than twenty-four hours, you have a bag of soup to look at.”) Peters inspected the bags—it was a relief to see that the monkeys were triple-bagged, anyway—and he decided to take them to Fort Detrick and worry about health laws afterward. “If the guy drove them back to Reston, I felt there would be a certain added risk to the population just from his driving them around in the van, and there would also be a delay in diagnosing them,” he said to me. “We felt that if we could quickly get a definite diagnosis of Ebola it would be in everyone’s favor.” They loaded the bags into the trunk of Peters’ car, a red Toyota. The monkeys depressed the rear end of his car. Peters didn’t see anything dripping. Nancy Jaax followed him to Fort Detrick.

When she arrived, she immediately suited up. First, she went into a locker room and put on a long-sleeved scrub suit and tucked her hair into a surgical cap. She put on a pair of white socks. Then she walked across the floor in her socks and waved a magnetic swipe-card across an entry sensor. A central computer at USAMRIID noted that Jaax, Nancy, was attempting entry into Containment Suite AA-5. Finding that she was cleared to enter the area, the computer beeped and unlocked the door. She went through the door into a negative-pressure Biosafety Level 3 staging area, the route into BL-4, the hot zone. There were two other pathologists in the staging area, and they and Nancy Jaax would work as buddies in the hot zone. She put on her inner surgical gloves and sealed them to the sleeves of her scrub suit with bands of sticky tape. Now she had one intact barrier between her and Nature. Her space suit was hanging on a peg, under ultraviolet lights. It was bright blue and was made of plastic. It had a soft plastic helmet with a clear faceplate. The suit had soft feet, like the feet in a bunny suit, and, attached at the wrists, rubber gloves. She stepped into the suit, fitted her hands into the gloves, and pulled the helmet over her head. She closed a steel zipper, followed by a Ziploc-type zipper. Her breath clouded the faceplate. Peering through condensation, she opened a supply air lock. Sitting in the air lock were the seven bagged monkeys. She picked up a couple of the bags and a box of necropsy tools, opened a door marked with a red toadshade, and stepped into the gray-zone air lock leading to Biosafety Level 4. In this air lock was a chemical shower. She opened the far door and walked into Biosafety Level 4, the hot zone. As she closed the air lock behind her, she pulled a chain, and the air lock began a decon cycle: an Envirochem shower ran in the chamber. That was to stop any backflow of organisms from the hot zone through the air lock.

From the ceiling of the hot room dangled an array of yellow air hoses. Jaax plugged a hose into her suit, and dry air cleared her faceplate. It made a loud rushing noise. People in BL-4 can hardly hear each other shout, and they often communicate by hand signals, like scuba divers. When you were in BL-4, even with a buddy, you were essentially alone. Jaax thought that it was like going into outer space.

She opened a stainless-steel-lined closet which was flooded with ultraviolet light, and removed a pair of rubber boots and pulled them on. She collected her necropsy tools and specimen containers and laid them beside a stainless-steel table. She untied a bag, and laid a crab-eating macaque on the table. Unclouded brown eyes stared at her. Some animal behaviorists think that monkeys are an alien consciousness unto themselves, where human rules don’t necessarily apply, and others think that monkeys’ minds and emotions work much like ours, since we are all primates. She slit the monkey’s abdomen with a scalpel, and then disposed of the scalpel in a sharps container. From this point on, she would use scissors. Scalpels are deadly instruments in a BL-4 hot suite. If you were to cut yourself with a hot scalpel, your boss would be filling out accident reports while you sat in the Slammer for the rest of your life—which might not be long.

The spleen was enlarged, but there were no obvious lesions inside this monkey. Then, at the base of the stomach, she found a ring of hemorrhages on the junction between the stomach and the small intestine—a lesion that is associated with simian hemorrhagic fever. She clipped samples of tissue and pressed them on glass slides. The slides were the only glass objects allowed in the hot zone. All laboratory beakers were plastic. A sliver of glass might pierce the suit and you, bringing into your bloodstream the replicative other. She worked slowly, rinsing her gloves often in Clorox. She was alone in a cocoon with the sound of her air.

While Nancy Jaax was in the hot room, a big meeting occurred in a conference room at USAMRIID. The meeting turned into a power struggle, between the Centers for Disease Control and the Army, over which institution would manage the Reston outbreak. Representing the C.D.C. were Dr. Joseph McCormick, who was then the chief of the Special Pathogens Branch at the C.D.C., and Dr. Frederick Murphy, who had first isolated Ebola. McCormick spoke for the C.D.C., and, according to the impression the USAMRIID people got, he said to them, in effect: Thanks for alerting us. The big boys are here now. You can turn this over to us. After all, the C.D.C. has a mandate for protecting the American population from infectious disease.

Colonel Peters resisted a takeover by the C.D.C. He and McCormick personally disliked each other, and the clash of personalities rapidly became institutional head-butting between the C.D.C. and the Army. At its heart, the argument concerned turf between doctors. Peters said to McCormick that the Army had appropriate containment suites for handling the organism and good tests that would reveal its presence in tissue. McCormick claimed that the C.D.C. had a better, newer technique for testing for Ebola. Peters replied that an ongoing epidemic is not the time to try to field-test a new technique. Peters added that USAMRIID was closer to the outbreak than the C.D.C. Peters hardly needed to add that those seven dead monkeys, even as he spoke, were being dissected in a hot suite: possession is nine-tenths of the law, and the Army had the meat. The participants agreed, finally, that the C.D.C. would manage the human-health aspects of the Ebola outbreak, while the Army would deal with the monkeys in Reston.

The next day, Peters walked into the office of Colonel Jerry Jaax, Nancy Jaax’s husband, and put him in charge of the group that would go to Reston. Jerry Jaax, in turn, called a meeting of military people and civilians at USAMRIID, and asked for volunteers to terminate the monkeys in Room H, take clinical samples, and sterilize the room. It was going to be a limited operation. They would leave the rest of the monkey house alone.

At five-thirty in the morning on Friday, December 1st, an Army biohazard group—all volunteers, mixed civilians and soldiers (including both officers and enlisted people), led by Jerry Jaax—assembled in a parking lot next to USAMRIID. Everyone wore civilian clothes, and they drove their own cars, to avoid attracting attention. They had filled three unmarked vans with equipment. The vans contained, among other things, Racal suits—the same type of lightweight suit that the Army team had used inside Kitum Cave. The group moved out, soon got stuck in rush-hour traffic, and didn’t arrive at the business park where the monkey house was situated until eight-thirty. They drove across a lawn and assembled in a secluded spot behind the monkey house, along a fringe of woods. The back side of the building presented a brick face, some narrow windows, and a glass door. The door was the insertion point.

It was a freezing, overcast day. From where they stood, they could see through the trees a day-care center with a playground, and they could hear shouts of children in the air. The operation would be carried out near children. Jerry Jaax had named Major Mark Haines, a veterinarian, the operational leader of the space-suited teams working inside the building. Haines, a Green Beret, had trained in the Green Berets’ scuba-diving school. Haines’ experience in underwater operations would prove helpful. A battery pack attached to each suit powered a blower that kept the suit pressurized with filtered air. The batteries had a life span of six hours, and people would have to be extracted from the hot area and decontaminated before their batteries failed, or they would be in trouble. Major Haines told the group that he wanted everyone to use the buddy system. Stick with your buddy and watch your buddy’s suit for rips or holes, he told them. Two of the group members were dating each other: they worked separately, following Army policy. Almost none of the teams’ members, including Haines and Jerry Jaax, had ever worn a Racal suit.

Nancy Jaax knew something about space suits, and she spoke to some of the team members. “Your suits are under pressure,” she said. “If you get a rip in your suit, you have to tape it shut right away, or you’ll lose your pressure, and contaminated air could flow inside the suit.” She held up a roll of brown sticky tape. “I wrap extra tape around my ankle, like this”—she demonstrated— “and then you can tear off a length of tape and use it to patch a hole in your suit. Be exquisitely careful. Know where your hands and body are at all times. If you get blood on your suit, stop and clean it off. Keep your gloves clean. With bloody gloves, you can’t see a hole in the glove.”

Suiting up proved to be difficult and embarrassing. You had to remove all your clothes, including your underwear, and then put on a surgical scrub suit. The teams rigged up a changing room inside one of the vans, screening it with sheets of plastic, but the women felt exposed. It was also bitterly cold. After you had put on your scrub suit, you went in through the insertion-point door to a staging area, and a support team there helped you put on your Racal suit.

The staging area led into a hallway deeper in the monkey house. They used this hallway as a makeshift air lock, or gray zone. It had doors at either end. One door led out to the staging area; the other door led into the monkey rooms. At no time were both doors to be opened simultaneously. The first two people to put on their suits and enter the air lock were Colonel Jerry Jaax and Major Mark Haines. They stood in the air lock for a moment, and then opened the door and entered the monkey area. Something had gone wrong with the heating system, and the temperature had soared above ninety in there. Jaax and Haines began to pour sweat—the Racal suits weren’t insulated—and their plastic head bubbles fogged up. The monkeys were subdued and hungry. Jaax and Haines walked up and down the hallways, going into each monkey room and checking the cages for dead or sick monkeys. They fed the monkeys their monkey biscuits. The monkeys hooted with excitement every time Jaax got near a biscuit bin. They found some chairs in a lounge and carried them into a hallway, where the volunteers could sit and rest while they sorted tubes of blood and loaded syringes with drugs. Jaax wanted to be sure that no one would reach inside a cage with a hypodermic syringe and get bitten by a monkey infected with Ebola. He had devised a mop handle with a U-shaped attachment on the end that would pin a monkey down in its cage. Then someone could stick the monkey with a syringe on the end of a pole.

Each insertion of a pair of buddies took twenty minutes. As the pairs were coming in, Jaax and Haines loaded some syringes with double doses of ketamine, an anesthetic. Then they went into Room H, the focus of the outbreak, and ran the mop handle into one cage after another, sticking each nervous animal with the pole syringe, and reloaded the pole with a full syringe after each injection. The monkeys began to collapse in their cages. When a monkey was down, Jaax injected the animal with a sedative, Rompun, which put it in a deep sleep.

The bleed teams set up bleed tables in a hallway, outside the view of any monkeys. (Monkeys get upset when they see euthanasia going on.) Haines would put an unconscious monkey on a bleed table, stick a needle in its thigh, and draw samples of blood. He would pass the monkey to Major Nathaniel Powell, Jr., a veterinarian, at a euthanasia table. Powell would lay the monkey out and give it an injection of T-61, a euthanasia agent, which killed the monkey. When the monkey’s breathing and heart had stopped, Powell would hand the monkey to Major Stephen Denny. He would open the monkey with scissors, snip out bits of spleen and liver, and put the samples in tubes. The other soldiers and the civilians put the monkeys in plastic biohazard bags, adding paper towels or kitty litter to soak up blood. They triple-bagged each monkey, washing the outside of each bag with Clorox, and then they loaded the bags into drums called hatboxes, which look like ice-cream containers but are blazed with biohazard symbols.

People grew tired and overheated in their suits, and some needed to go to the bathroom. As the day wore on, they began coming out in pairs through the air lock. A gray team, also wearing Racal suits, stood in the air lock between the two worlds and sprayed each person’s suit with Clorox. Then the person went into the staging area, where the support team peeled off the suit, and the person climbed into the van and stripped to the skin, a shivering tropical primate. The men and women put on their clothes and stood around on the grass, looking pale, weak, and thoughtful. By nightfall, all the monkeys in Room H had been put to death.

That weekend, Dan Dalgard caught up on his diary. “Retirement as a clock repairman looks better each day,” he wrote. He worried that television crews would show up on Monday morning, and he ordered the Hazleton animal caretakers, who were still entering the Reston monkey unit to feed the surviving monkeys but were now wearing respirators and overalls, not to go outside the building with their protective equipment on. He did not want images of Hazleton monkey workers wearing what looked like gas masks to appear on the evening news.

He arrived at the monkey unit early on Monday morning, and was parking his car when he saw a Hazleton animal caretaker, who will here be called Francis Milton, standing out on the lawn by the main entrance wearing his respirator and suit. Dalgard was furious. He jumped out of his car. Suddenly, Milton pulled off his respirator, knelt in the grass, and vomited. Dalgard was “scared shitless,” he told me later. Milton developed the dry heaves. Dalgard helped him to his feet, took him indoors, and had him lie down on a couch. They couldn’t find a thermometer. Someone ran to a drugstore and bought one. Milton had a fever of a hundred and one. He was shaky and felt faint. He appeared to be breaking with Ebola. He did not seem afraid; he told people that he had been previously saved, and had put his life in the hands of Our Lord. They called an ambulance. Just as it showed up, so did television crews. The ambulance, chased by television vans, took Milton to Fairfax Hospital, where he was put into an isolation ward.

Dalgard now had two employees in the hospital—Purdy with a heart attack and Milton with a fever—and either of them could be breaking with Ebola. He decided that he must order the destruction of all the monkeys. The time had come to evacuate the building and turn it over to the Army. He called Colonel Peters at Fort Detrick. Peters asked Dalgard to send him a letter ceding control of the building to the Army. Dalgard sent it immediately by fax. Peters showed it to General Russell. Peters saw a need for clarity and speed. “You reach a point where you need to make a decision,” Peters explained to me. Dalgard, in his letter, had asked the Army to assume responsibility for any liability that would arise after the Army took over. Peters refused to assume liability. Dalgard backed down; they signed the letter; Dalgard evacuated and locked the building; a Hazleton courier drove the keys to Fort Detrick; and the building fell under the control of the Army.

The next day—Tuesday—the biohazard teams returned, with their unmarked vans, and deployed in the grassy area behind the building. The teams began to suit up. Before they went inside, Major Haines, the Green Beret, gave them a talk. By his later account, his words went this way: “You are going to euthanize a whole building full of animals. This is not a fun operation. You must consider these animals as beings of a kind. Don’t go in and play with the monkeys. I don’t want to hear laughing and joking around the animals. I can be hard. Remember the veterinarian’s creed: You have a responsibility to animals and you have a responsibility to science. These animals gave their lives to science. They were caught up in this thing; it’s not their fault; they had nothing to do with it. Go in by twos. Never hand a used needle to another person. If a needle comes out of its cap, it goes straight into an animal, and then don’t recap it, because you could stick yourself. Put the used syringe straight into a disposal container. If you get tired, tell your supervisor, and we’ll decon you out.”

It took three days to kill all the monkeys, and the teams did it room by room. The most dangerous job fell to Jerry Jaax. That was to inject conscious monkeys with the first anesthetic, and not get bitten. A sergeant named Thomas Amen stayed at Jaax’s side during most of the operation. He and Jaax took turns pinning the monkeys with the mop handle and giving them injections with the pole syringe. The lowest banks of cages were at floor level and were often dark. Jaax, who is a tall man, had to get down on his knees to peer inside them. He could hardly see anything through his head bubble. He would pick out the shape of a monkey in the back of a cage, pin it down, and then Sergeant Amen would ease the pole syringe into the cage, aiming for the thigh. There would be screeches and a wild commotion, the monkey shrieking “Kra, kra! ” Jaax’s knees hurt and he could hardly stand up after a day of injecting monkeys. He was one of the last to be deconned out at the end of each day, and Mark Haines remarked later that when Jerry Jaax took off his Racal suit he looked ten years older.

At Fort Detrick, Nancy Jaax stayed up late every night, dissecting monkeys and preserving their tissues. Nancy and Jerry didn’t speak much about the job to their children—a son and a daughter, who were both in middle school. The children hardly saw their parents during the emergency. On December 7th, Nancy’s father died, in Wichita. Jerry urged her to go home for the funeral. She flew home alone, reflecting that she had not been there to hold her father’s hand.

Inside the Reston monkey facility, the bleed team set up a table in an empty monkey room, where there was a water faucet and a floor drain. The constant sampling of monkey blood and tissues generated much blood; they washed it down the drain with Clorox. As the nuking went on, by the second and third days you could see exhausted soldiers and civilians in suits, men and women, their head bubbles clouded with condensation, sitting in the chairs in the main hallway, loading syringes with T-61 and sorting boxes full of blood tubes. Some talked loudly, to be heard over the whine of their blowers, and others just stared at the walls.

When the monkeys were dead, the teams cleared out, and locked the building. They had collected a total of thirty-five hundred clinical samples, but nobody had stuck himself with a needle or received a bite. Then the decon team arrived. The rooms and halls were bloodstained and strewn with medical packaging, monkey biscuits, and monkey feces. Every object and surface had to be presumed lethally hot. The decon team wore Racal suits and worked slowly. They washed the walls with Clorox bleach. They bagged the medical debris, and washed feces out of corners with bleach and shoveled it into bags. The bagged monkeys were delivered to Dalgard’s people, to be burned at a Hazleton incinerator. Using silver duct tape, the decon teams taped all the doors and windows shut and taped sheets of plastic over vent openings, first inside the building and then outside, until they had made the building airtight.

Finally, on December 18th, the decon team set out patches of paper saturated with spores of a harmless bacterium known as Bacillus subtilis niger, scattering them all around the monkey house. These spores are hard to kill. It is believed that a decon job that kills niger will kill anything. The team had brought thirty-nine Sunbeam electric frying pans. Sunbeam frying pans are the Army’s tool of choice for a decon job. They plugged the frying pans into heavy-duty electrical outlets all around the monkey building, which were wired to a master switch. Into each Sunbeam they dropped a handful of paraformaldehyde crystals. They dialled the pans to “high.” At 18:00 hours on December 18th, someone threw the master switch, and the Sunbeams began to cook, releasing formaldehyde gas. The building’s doors, windows, and vents, having been taped, prevented the gas from escaping. Three days later, the decon team, again wearing Racal suits, went back inside the building and collected the spore samples. The Sunbeam treatment had killed the niger. Total, unequivocal sterilization of a room is difficult to achieve and nearly impossible to verify, but a Sunbeam cookout that exterminates niger implies success. The building had been nuked. For a short while, the Reston Primate Quarantine Unit was probably the only building in the world where nothing lived, nothing at all.

Tom Geisbert and Peter Jahrling, who had breathed Ebola Reston virus from a flask, worked around the clock for weeks, testing monkey blood and tissues. As the days went by and they did not develop headaches, their worry subsided. They were encouraged by the fact that Dan Dalgard had not developed Ebola-virus infection. He had been dissecting hot monkeys weeks before the Army found Ebola in them, and he was fine. In the end, neither Geisbert nor Jahrling came down with Ebola, and neither showed immunological signs of having been exposed to the virus. As for Francis Milton, the Hazleton animal caretaker who had vomited on the lawn, he recovered quickly. It seemed that Milton had had influenza—or, possibly, an extremely mild case of Ebola Reston. Later, Milton developed antibodies to Ebola Reston. That means he had become infected with the strain. The virus had multiplied inside him, but he had not developed clinical disease, except, perhaps, nausea and fever—if, indeed, his illness came from Ebola rather than flu. Milton did not give Ebola to anyone else. As for Purdy, the animal caretaker who had had a heart attack, he recovered normally.

After the decon team left, Hazleton Research Products took the building back. In January, 1990, the company restocked the building with monkeys, which it had bought from the same Philippine exporter that supplied the earlier batches of sick monkeys. A few weeks after the restocking, Ebola Reston virus mixed with simian hemorrhagic fever again broke out in the monkey building. It seemed that the Ebola Reston virus had been circulating at the Philippine exporter’s compound in Mindanao.

This time, Dan Dalgard did not turn the Reston monkey house over to the Army, but he did let the Army take samples back to USAMRIID. Since no human illness had resulted from the first outbreak, Dalgard decided to try to contain the disease room by room. When disease broke out in a room, he sacrificed all the monkeys in that room. But the virus began appearing in room after room, accompanied by respiratory signs, such as coughing, bloody sputum, and hemorrhagic pneumonia, and by March most of the monkeys were dead. Hazleton was renting the building from a commercial landlord. Not surprisingly, relations between Hazleton and the landlord did not improve during the Army nuking and the second outbreak of Ebola. Hazleton vacated the building after the second outbreak, and to this day it stands empty.

Perhaps the most surprising fact about the Reston emergence is that it has not resulted in any obvious human illness or death. There was, however, a subtle and perhaps sinister effect. Six Hazleton employees had close contact with the sick monkeys, including Dan Dalgard. Of those six men, four—all but Dalgard and a supervisor—developed antibodies to the virus in their bloodstream. That means that the virus replicated successfully in the four men’s tissues. One of the four, a man who will here be called John Coleus, cut his finger with a scalpel while performing a necropsy on a monkey that had died of Ebola Reston. It happened during the second outbreak, in February, 1990. “We were frankly fearful that he had bought the farm,” Peter Jahrling said to me. But John Coleus didn’t even get sick. Why John Coleus didn’t die of Ebola is one of the great mysteries of the Reston outbreak. He was certainly infected with Ebola—the virus had multiplied in him—yet he showed no ill effects. As for the three other men who caught Ebola Reston, it seems that they must have picked up the virus through the air. They were using water hoses to clean the cages, and they may have breathed droplets of monkey waste or monkey mucus into their lungs. To date, none of the four men have shown any clinical symptoms of illness. Ebola Reston virus infects human beings but apparently doesn’t make them sick—or possibly it gives them a flu-like illness. Yet it appears to be absolutely deadly to monkeys.

Ebola Reston virus is an extremely close relative of Ebola Zaire, the hot strain. It may be that Ebola Reston is a variant of Ebola Zaire; perhaps a mutation rendered it harmless to human beings. It may be that Ebola Reston is a Southeast Asian cousin of Ebola Zaire. Epidemiologists visited the Philippine monkey-export facility in Mindanao and found that none of the employees there had suffered a serious unknown illness in the year preceding the Reston emergence. Ebola Reston and Ebola Zaire look the same in an electron microscope. A molecular biologist at the C.D.C. named Anthony Sanchez has begun to analyze the Ebola virus’s genetic sequences. He has found that Ebola Reston is, genetically, very close to Ebola Zaire. “I term them kissing cousins,” he said to me. “But I can’t put my finger on why Reston is apparently apathogenic in human beings and doesn’t make us sick.”

In March, 1990, right after the second Reston outbreak, the C.D.C. slapped a heavy set of restrictions on monkey importers, tightening the testing and quarantine procedures. The C.D.C. also temporarily revoked the licenses of three companies—Hazleton Research Products, the Charles River Primates Corporation, and Worldwide Primates—charging those companies with violating quarantine rules. The C.D.C.’s actions effectively stopped the importation of monkeys into the United States for several months. The total loss to Hazleton ran into the millions of dollars. Monkeys are worth money. Crab-eating macaques fetched around five hundred dollars apiece before the Reston outbreak; since then, government regulations and a monkey shortage have driven the price to fifteen hundred dollars. Despite the C.D.C.’s action against Hazleton, scientists at USAMRIID, and even some at the C.D.C., give Dalgard and his company high praise for making the decision to hand the monkey facility over to the Army, which cost the company millions but seemed essential for the safety of the American population. “It was hard for Hazleton, but they did the right thing,” Peter Jahrling said to me.

Jahrling, an inhaler of Ebola who lived to tell about it, is now the acting chief of virology at USAMRIID. He is also credited, along with Tom Geisbert, with having performed the first laboratory isolation and characterization of the Ebola Reston strain. This recognition gives Jahrling the right to name it; he hasn’t decided on a name. One day, in his office, he showed me a photograph of some Ebola virus particles. They looked as if they had been cooked al dente and would make a tempting first course at a trattoria in Rome. “Look at this honker. Look at this long sucker here,” Jahrling said, his finger tracing a spaghetto. “It’s Res— Oh, I was about to say it’s Reston, but it isn’t. It’s Zaire. The point is, you can’t easily tell the difference between them by looking. It brings you back to a philosophical question: Why is the Zaire stuff hot? Why isn’t Reston hot, when they’re so close to each other? The Ebola Reston virus is almost certainly transmitted by some airborne route. Those Hazleton workers who developed antibodies to the virus—I’m pretty sure they got the virus through the air.”

“Did we dodge a bullet?” I asked.

“I don’t think we did,” he said. “The bullet hit us. We were just lucky that the bullet we took was a rubber bullet from a .22 rather than a dumdum bullet from a .45. My concern is that people are saying, ‘Whew, we dodged a bullet.’ And the next time they see Ebola in a microscope they’ll say, ‘Aw, it’s just Reston,’ and they’ll take it outside a containment facility. And we’ll get whacked in the forehead when the stuff turns out not to be Reston but its big brother.”

Karl Johnson, the leader of the team that isolated and named the Ebola virus, is sitting in a swale of dry grass on the bank of the Bighorn River. Something screams on the opposite bank. “Hear that pheasant? That’s what I like about the Bighorn,” he says. He peers across the water, where insects are hatching from the river’s surface. “Huh! We’ve got two different emergences going on here.”

I look carefully and see two swarms of insects coming off the water. One type of insect is flying upstream, into the wind; the other type is being blown downstream. The clouds are passing through each other, two interpenetrative rivers of insects flowing above the river of water. “The ones that are flying upstream are little tiny mayflies called tricos,” Johnson says. “The others are the baetises. They have really long tails. These insects spend a year or more at the bottom of the river as nymphs. Then they pupate and rapidly emerge from the water and fly away as adults. The adults molt into spinners, which is the egg-laying form, and the spinners lay their eggs on the surface of the river and die. The process from emergence to dying can happen fast—the whole thing might take a couple of hours. These hatchers are like emerging viruses. The viruses have been on the earth a long, long time. Invisible. In the river, you might say.” Johnson tells me that the word “emerge” comes from the Latin word emergere. In Webster’s unabridged dictionary, its first meaning is: “To rise from . . . an enveloping fluid.” He says, “It means to come through another medium. Most of the emerging viruses are being transmitted to man from animals. Coming through another medium. There’s been this incredible damned surge of people on our planet. There’s been a human population explosion and a human invasion of tropical habitats. There are just too many people entering too many ecosystems and violating them. People stumble into something and get sick.”

Johnson stands up and knots to his line a tiny fly that looks like a dead spinner, a canapé for a trout. Bufflehead ducks are diving at the head of the pool, and a trout rises and flops, transmitting rings into the water that spread and die, absorbed in the filiations of the Bighorn.

“Do you find viruses beautiful?”

“Oh, yeah,” he says softly. “Looking at Ebola under an electron microscope is like looking at a gorgeously wrought ice castle. The thing is so cold. So totally pure. In Bolivia, we found out that the reservoir of the Machupo virus is a wild mouse. Machupo is fundamentally a sexually transmitted infection in a mouse. These Bolivian mice live in demes, which are like villages. They copulate frequently. When the mouse population expands to the point where there is contact among the demes, you have a sexually transmitted plague of Machupo in the mice, and the population crashes. The Machupo virus is a force that keeps the mouse population from going out of control and using up its food supply. Machupo benefits the mouse as a species, because when the demes touch, the population gets thinned out. This is Nature. And I happen to think it is one of the loveliest biological structures I’ve ever seen.”

“It sounds like AIDS,” I say.

“You’re damned right. AIDS is that way for us. As a biologist, from a deeply philosophical viewpoint, I don’t think there’s any difference. As a physician, of course, I can’t turn my back on another human being.”

This past week in Washington, the Institute of Medicine, which is chartered by the National Academy of Sciences, called a news conference and released a frightening report entitled “Emerging Infections.” The report was two years in the making. Under the heading “Trouble Ahead,” the report described the Reston emergence as a classic example of “the potential of foreign disease agents to enter the United States.” The Reston emergence scared a lot of epidemiologists.

The Institute of Medicine report essentially warns us to stay tuned. It says that not only emerging viruses but also mutant bacteria, such as the strains that cause multi-drug-resistant tuberculosis, and protozoans, such as mutant strains of malaria, have become major and growing threats to the American population. The report says, “We can also be confident that new diseases will emerge, although it is impossible to predict their individual emergence in time and place.” The Institute of Medicine finds that there has been a general breakdown in the public health system in the United States. We lack the forces to deal with a monster, at the very time when a monster could appear—especially given the emergence of H.I.V.

In its two years of deliberation, the committee came up with some recommendations: We need to have a national and worldwide surveillance system to identify emergences as they happen. (If we had had such a system in place fifteen years ago, we might have seen AIDS hatching off the river, as it were, perhaps in Central Africa, and we might have been able to save thousands of American lives.) We need a modernized and strengthened vaccine program, which would include a “surge” capacity for vaccine development, to respond to an emergency. We need better preventive medicine, to keep people from spreading emergent infectious diseases. And we need to train more field epidemiologists, since they are the detectives who help us find and know our enemies.

One of the authors of the Institute of Medicine report is a virologist named Stephen Morse. In the course of writing this account, I dropped in on him several times at Rockefeller University, in Manhattan. Morse is a voluble, bearded figure, who inhabits a paper-jammed lair on a hallway that reeks of urine from rabbits and mice. (Viruses need to grow in cells.) One day an unpleasant thought crossed my mind, and I asked Morse if an emerging virus could wipe out our species.

“Isn’t H.I.V. enough?” he asked. He said that H.I.V. might actually do the job. There has been some debate, recently, about whether H.I.V. could mutate into an airborne disease, like influenza. Then AIDS would suddenly become AIDS-flu. It would circle the globe in a flash. The case mortality in AIDS seems to be close to a hundred per cent. “The H.I.V. particle does get into the lung,” Morse explained to me. “There is no reason in principle why H.I.V. couldn’t spread by the respiratory route. Many viruses that are closely related to H.I.V., such as the Visna virus, which is a fatal immune-deficiency virus of sheep, do spread through a cough. The sheep cough, and the virus is aerosolized. Indeed, primary H.I.V. infection—when you first get infected—has been associated with a flu-like illness, with upper respiratory system involvement: coughing, wheezing, and so forth.” He added that if H.I.V. did mutate into AIDS-flu, the question was whether it would remain fatal. Would it kill its human hosts or would it evolve toward something more benign, something like a nasty but survivable cold? “The human population is genetically diverse, and I have a hard time imagining everyone getting wiped out by a virus,” he said. “But if one in three people on earth were killed—something like the Black Death in the late Middle Ages—the breakdown of social organization could be just as deadly, almost a species-threatening event.”

I drove to Reston one day in autumn to see the former Primate Quarantine Unit, and stopped my car in front of the building. A sycamore tree on the lawn dropped an occasional leaf. The place was as quiet as a tomb. “For Lease” signs sat in front of many of the offices around the parking lot. I sensed the presence not of a virus but of financial illness—signs of convalescence from the eighties, like your skin peeling off after a bad fever. I parked beside a school and walked across the grassy area behind the former monkey house until I reached the glass door that had been the insertion point. It was locked. Shreds of silver duct tape dangled from the door’s edges. I looked inside and saw a floor mottled with reddish-brown stains. A sign on an inner wall said “Clean up your own mess.” I discerned the air-lock corridor—the gray zone through which the teams had passed into the hot zone. It had unpainted cinder-block walls: the ideal gray zone.

My feet rustled through shreds of plastic in the grass. I heard a ball bounce, and saw a boy dribbling a basketball in the school playground. The ball cast rubbery echoes off the buildings. I walked along the back wall of the former monkey house until I came to a window. Inside the building, climbing vines had rioted, and had pressed themselves against the inside of the glass. The vine was Tartarian honeysuckle, a weed that grows in waste places and abandoned ground. I couldn’t see through the leaves into the former hot zone. I walked around to the side of the building, and found another glass door, beribboned with tape. I pressed my nose against the glass and cupped my hands around my eyes, and saw a bucket smeared with a dry brown crust. It looked like monkey excrement. I guessed that it had been stirred with Clorox. A spider had strung a web between a wall and the bucket of shit, and had dropped husks of flies and yellow jackets on the floor. Ebola had risen in these rooms, flashed its colors, replicated, and subsided into the forest. ♦