by Reid Wilson
The first situational report issued by WHO, three days later, showed just how quickly the virus had spread: it showed eighty-six total cases of Ebola in Guinea and fifty-nine deaths.
By the time the world knew that the flame spreading across the Forest Region was Ebola, eight villages and cities were on fire. And while earlier outbreaks quickly ebbed for lack of new hosts, this epidemic was about to find new fuel. A few days earlier, the same day the Ebola-tainted blood left Conakry for Paris, a trader who made his living exchanging goods in the Forest Region arrived in Conakry.11 He was not feeling well; he had a fever.
TWO
A Mysterious Killer
MOST VIRUSES, VIEWED UNDER a microscope, have a kind of beauty to them. Some are round, others crystalline, many symmetrical. They inspire an appreciation of the beauty of nature, even if their appearance masks their danger.
The Ebola virus is not beautiful. A member of the filovirus family, it extends in a long, unbroken line, filaments sprouting out like stubbly hairs, wrapping around itself like a coiled snake. It is made of only about 19,000 segments of RNA, the genetic code that governs its existence, a relatively tiny number by comparison to other viruses. A single virion is about 1,000 nanometers in length; it would take about 100 Ebola virions, laid end to end, to match the diameter of a single human hair. Not much is known about Ebola when it is not present in humans, including the identity of its reservoir host.
The Ebola virus, like all viruses, is an accident of evolution. It lives benignly in its reservoir host, with no ill effects, just like the thousands of organisms that inhabit a healthy human. It is not malicious, it does not seek out human life to end. Rather, it seeks an environment in which to replicate itself to survive. But there is something in the genetic language of the virus, something in those 19,000 segments of RNA, that orders it to operate differently when it comes into contact with human cells.
The process of a virus jumping from animals to humans is called zoonosis. About 60 percent of all infectious diseases in human history have come from animals—everything from the Bubonic plague, spread by fleas that live on rats, to Lyme disease, spread by tics, and malaria and the Zika virus, harbored in mosquitoes. The moment zoonosis actually takes place is called a spillover.1
Once the spillover occurs and the virus enters the human body, a virion seeks out a red blood cell, which it snags with its tiny filaments. The virion is pulled inside its cell, where it begins to reproduce at a breathtaking pace. Within eighteen hours, the number of Ebola virions in an infected cell reaches a critical mass, causing the cell to erupt and shoot thousands of new virions into the bloodstream, where they seek out other cells to infect. They are happiest when they find macrophages, white blood cells that scoop up the remains of dying cells, along with any foreign disease that might have killed them. The Ebola virus, in effect, turns the body’s garbage trucks against it—each macrophage another log on the fire, ready to burn, explode—and further spread the invader.
The disease attacks virtually every part of the human body, with the exception of bones and skeletal muscles. It finds particularly attractive cells that line blood vessels in the liver. The infected cells die, dissolving tissues inside the human body.
Ebola is deadly, but compared with other viruses it is relatively difficult to transmit from one human to another. Only when the bodily fluids of an infected person come into contact with a mucus membrane of an uninfected person—whether through the eyeball, the mouth, or an open cut—can the virus jump. Someone who has Ebola but shows no symptoms is not contagious. Even when they are contagious, the disease must travel inside bodily fluids; it is not airborne.
But the virus’s ravenous appetite for human tissue means a victim becomes more and more infectious as Ebola finds more and more sustenance. At the moment of death, an infected body is at its most dangerous. Touching the body of an Ebola victim is like stepping on a biological land mine.
In modern history, major outbreaks of hemorrhagic fevers like Ebola have only erupted a handful of times. The first occurred in 1967, when a handful of workers in Marburg, Frankfurt, and Belgrade fell ill after handling infected monkey tissues. Seven of the thirty-one people who fell ill in that first outbreak—a filovirus that came to be known as Marburg—died.
But filoviruses are tens of thousands, maybe millions, of years old. Some historians believe the plague described by the Greek historian Thucydides, which wiped out thousands of Athenians, may have been Ebola. The symptoms Thucydides described match those of Ebola:
People in good health were all of a sudden attacked by violent heats in the head, and redness and inflammation in the eyes, the inward parts, such as the throat or tongue, becoming bloody and emitting an unnatural and fetid breath.… When it fixed in the stomach, it upset it; and discharges of bile of every kind named by physicians ensued, accompanied by very great distress.… Internally it burned so that the patient could not bear to have on him clothing or linen even of the very lightest description; or indeed to be otherwise than stark naked.
Thucydides, who contracted and survived the disease himself, said the plague began “in the parts of Ethiopia above Egypt, and thence descended into Egypt and Libya and into most of the King’s country.”2
The first confirmed cases of Ebola in modern history occurred nearly forty years before Emile fell ill, more than 3,000 miles away from West Africa.
In the winter months of 1976, in the small village of Yambuku, in what was then Zaire, Mabalo Lokela fell ill. Lokela was the popular headmaster of Yambuku’s only school. When he was taken to the small Catholic mission hospital, run by a team of Belgian nuns who had provided medical treatment to the 60,000 or so residents of the surrounding area since 1935, his fever was spiking. Fluids were leaking from his body faster than medical workers could replace them. He was dead before anyone had time to consider what had killed him.
Then the first wave began. Nearly two dozen patients crowded the hospital, overwhelming doctors who had no idea what they were seeing. The medical staff tried everything in their limited arsenal, from aspirin to chloroquine, nivaquine, stimulants, caffeine, coagulants, anything they could get their hands on. Within a week, fourteen of the first twenty or so infected villagers were dead. They died so fast that the district medical director, making his first report of the outbreak to his superiors in Kinshasa, had to cross out the number of dead. Two more patients had died in the few hours it took him to travel the short distance between Yambuku and his district headquarters, where he could report back to his superiors. Within a month, the hospital had run out of antibiotics. The scene was horrifying; blood was everywhere—in projectile vomit, in explosive diarrhea, oozing from noses and eyes. Doctors, those few who had not fallen ill themselves, sent a message to the capital Kinshasa, begging for help. Lokela’s wife, eight months pregnant when her husband first visited the hospital, was one of the few survivors.3
By the time an international team of virologists and biologists arrived from the United States, France, Canada, Belgium, and South Africa, along with officials from Zaire’s Ministry of Health, a month later, the hospital was closed. Most of the doctors were dead. A medical official from the neighboring province told the Westerners that the disease had already spread through at least forty-four villages within fifty miles of Yambuku in less than a month.
To the scientists who arrived in the new hot zone, led by a pioneering epidemiologist from the Centers for Disease Control and Prevention (CDC), the disease looked familiar. It was related to Marburg, the virus first identified almost a decade before in Europe.
But clearly, this bug was more virulent. By the time the international team arrived in October, when the outbreak was dying down, whatever they were looking at had killed 88 percent of its victims—280 of 318 cases—a mortality rate unheard of since the Black Death of the fourteenth century.
The disease was named for the small river that ran near the village, a tributary of a tributary of the mighty Congo, hardly identified on any b
ut the most detailed maps: the Ebola River.
At almost the same time—in fact, just a few months before the outbreak in Zaire—another hemorrhagic fever had announced itself a few hundred miles away, in the town of Nzara just across Zaire’s border with Sudan. (Today, Zaire is the Democratic Republic of the Congo. Nzara has been drawn in to South Sudan, the world’s newest nation.) This time, it was workers in a cotton factory who presented the first cases. When the fire burned out, about 53 percent of those infected in the towns of Nzara, Maridi, Tembura, and Juba had died.
Lab tests showed that the two diseases were related, and initially, scientists at the World Health Organization believed the outbreak in Sudan may have sparked the outbreak in Zaire. Eventually, they realized they were looking at two closely related, but distinct, bugs: one would later be named Ebola hemorrhagic fever, abbreviated EBOV by infectious disease researchers; the other would be called Sudan virus, or SUDV, of the same Ebola virus family. (Later, the EBOV disease dropped the “hemorrhagic” from its name; hemorrhages only happened in a small handful of cases.) Subsequent outbreaks would identify two more strains, Bundibugyo virus (BDBV) and Reston virus (RESTV), all closely related but genetically distinct.
Those diseases spread through direct contact with bodily fluids, and evolution has conspired to create conditions for that contact—vomiting, bleeding, and diarrhea all contain deadly amounts of the virus. That puts health-care workers who treat patients at particular risk, though the virus can spread through something as simple as touching one’s eye. (Thucydides wrote that physicians in Athens who attempted to treat the sick were among the most vulnerable to the disease.)
After the initial outbreaks in Zaire and Sudan, the virus seemed to disappear, with only the occasional flare-up. A recurrence in Nzara and Maridi, sites of the 1976 outbreak in Sudan, claimed 22 lives three years later. EBOV waited until 1994 to announce its presence once again, this time in Gabon, where 31 of the 52 infected patients died; doctors initially misdiagnosed the disease as yellow fever. The following year, 254 people died—81 percent of those infected—in an outbreak in Kikwit, Zaire. In 1996, 21 of 37 people who fell ill in Mayibout, Gabon, died. Gabon suffered another outbreak in 1997, when 45 of 60 people infected in Booue died.4
Those early outbreaks in central Africa provided some clues to researchers investigating this new pathogen, hints that the virus lived somewhere in the jungle. Yambuku is buried deep in the Congolese forest. The first patient to fall ill in Kikwit worked in the forest. In Mayibout, 19 of the 21 who died had handled a chimpanzee found dead in the forest by a band of hunters. (Chimpanzees and apes, so genetically similar to humans, are also highly susceptible to Ebola.) The first victim in Booue was also a hunter from a nearby forest camp where a dead chimpanzee had been found.
After two decades lying dormant, the Ebola virus became a regular, if still rare, crisis for public health officials. Uganda experienced its first outbreak, of the Sudan strain of the virus, in 2000. It arrived in Congo, along the border with Gabon, in 2001, then twice more in 2002 and 2003. Between 2007 and 2009, two outbreaks hit the Democratic Republic of the Congo (renamed in 1997) and another hit Uganda.
The outbreaks caused a terrifying mortality rate. The EBOV strain took the highest tolls, killing between 60 percent and 90 percent of those infected. SUDV caused death in between 40 percent and 60 percent of the infected. BDBV killed fewer than half of its victims, between 25 percent and 47 percent, still a shockingly high number. By comparison, Spanish influenza, which is estimated to have killed around 40 million people from 1918 to 1920 had a mortality rate of just 2.5 percent.5
But even with yearly outbreaks, Ebola seemed contained. The towns that suffered were deep in the bush, hours removed from their nearest neighbors over rough terrain or long, winding rivers. The virus killed so fast that only occasionally did anyone infected make it far enough away from the epicenter of an outbreak, called a hot zone, to threaten other populations. Only once did the virus cross into a wholly new country—in 1996, when an infected medical professional who had fought the outbreak at Mayibout got on a plane to South Africa. He survived, but a South African nurse who treated him died.6
For the most part, the Ebola virus followed a clear pattern: It would flare up, usually taking root in someone who lived or worked in the forest. Local health workers, unprepared for a disease they usually had no experience with, were primarily at risk, as was the index patient’s immediate family. But after a handful of cases, and usually after the arrival of international experts who began establishing a familiar routine of quarantines, the virus would find itself at a dead end, burned out among a small population. There was virtually no risk that Ebola could emerge from the jungles of central Africa to threaten any major population centers.
Still, such a frightening virus was almost certain to catch the imagination of the public. The author Richard Preston helped popularize Ebola in his 1994 book The Hot Zone, which described terrifyingly gory scenes of human bodies melting away from a tropical pathogen with no known cure.
In his best seller, Preston included the story of a strain of the Ebola virus that had in fact arrived on American soil a few years before. In 1989, monkeys imported from a facility in the Philippines began dying at a warehouse in Reston, Virginia, just miles from Washington, D.C. Those monkeys were found to have the RESTV strain of the disease, though another genetic quirk appears to have rendered that version of the disease harmless to humans. Three workers at the export facility in Manila had antibodies in their blood; the next year, another monkey die-off showed that the disease was present in four Americans in Virginia and Texas. None of those workers showed any symptoms.
Preston’s book inspired the 1995 hit movie Outbreak—but his description of the disease borrowed liberally from the imagination, overstating both its dangers and its symptoms. To this day, twenty years later, mentioning Preston’s name to a virologist or an epidemiologist elicits a shake of the head, an expletive, or both.
Disease experts had studied Ebola since its very first appearances in 1976. But two disasters seemingly unrelated to tropical diseases—the September 11, 2001, terrorist attacks on New York and Washington and the appearance, just weeks later, of mail laced with anthrax sent to several American newspapers and to members of Congress—gave new urgency to the cause. Suddenly, America faced the prospect of bioterrorism attacks, specific and very contagious pathogens unleashed on the public in confined spaces, like subways or theaters. There was evidence, too, that at least one other nation had pursued research into Ebola, possibly for use in biological weapons: lab workers in Russia had been infected, most likely by accidental needle pricks, in 1996 and 2004. In both cases, those workers died.
Fears of biological threats from abroad spurred the American government to begin studying spreadable diseases with renewed vigor. Working in sealed labs at the Centers for Disease Control and Prevention in Atlanta, the U.S. Army Medical Research Institute for Infectious Diseases (USAMRIID) at Fort Detrick, Maryland, and in a remote National Institutes of Health facility in Hamilton, Montana, scientists studied what they called Category A agents, highly infectious pathogens that could cause widespread outbreaks like smallpox, botulism, tularemia, plague, and hemorrhagic fevers like Marburg, Lassa, and Ebola.
“Our work on Ebola antedated, by many years, the Ebola outbreak, because it was part of something that we started in earnest right after 9/11, when the anthrax attacks occurred in the fall of 2001,” said Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, a division of the National Institutes of Health (NIH). “We put together a program to better understand diseases, at that time based on the perceived need for defense against bioweapons that the Soviet Union had developed during the Cold War.”
Much of that work took place at USAMRIID, housed in a patchwork series of stitched-together buildings behind several layers of security at Fort Detrick. Originally designed for just three hundred of the Army’s top scientists, it is now ho
me to about a thousand experts and administrators, some crammed into offices that were once called temporary, when they were first installed decades ago.
Below the office space, tucked away off cramped hallways where biohazard suits hang on racks like overcoats for a moon mission, are the laboratories where some of the deadliest diseases in the world are studied. There are four levels of biosafety suites, requiring various protections and protocols depending on how dangerous the substances inside may be. Biosafety level one, or BSL-1, is the equivalent of a classroom, where no special precautions are needed. BSL-2 requires a lab coat, though nothing too hazardous is present.
BSL-3 suites are where the truly dangerous diseases start showing up. Researchers use respirators, masks, and extra gloves to study diseases like Rift Valley Fever, yellow fever, West Nile virus, and severe acute respiratory syndrome (SARS)—diseases that have the potential to be deadly, but for which there are known cures, vaccines, or treatments.
Studying diseases that have no known cures is reserved for specially trained researchers under biosafety level-four conditions, with heavy security and even heavier protections. The BSL-4 suites, visible along white, sterile hallways through double-paned glass, are where Ebola and Marburg live.
Anyone entering one of those suites must pass through three levels of security—a fingerprint scan and two pads that demand unique pin codes—before even entering a changing room. Once there, a researcher will don scrubs before spending several minutes testing a pressurized suit, first visually, and then for any pressure loss. A double submarine door held shut by 6,000 pounds of pressure still stands between the dressing room and the laboratory; neither door can be open when the other is, to ensure a constant barrier between pathogens and the outside world. There are similar precautions inside the laboratory. The room itself has a negative airflow, meaning air is always being sucked in, never pumped directly out. All liquids that leave the laboratory zip through high-pressure lines and come into contact several times with chlorine; both the pressure and the chlorine will kill any potential pathogens left alive. Wastewater is then pumped to a separate holding tank, where it encounters even more chlorine. When lab work is finished, a researcher spends seven minutes in a shower, sprayed down by both water and microchemicals that can kill any living specimen that might remain on the suit.