Crisis in the Red Zone

by Richard Preston

  Spencer ended up isolated in a high-biocontainment unit at Bellevue Hospital, where he spent nineteen days with the virus, and ultimately recovered, having received top-notch care by a Bellevue medical team. The public and media got very nervous about how he had ridden the subway and gone many places in the city while the virus was in his body but he didn’t have a fever. Spencer felt that public health authorities and the media had overblown the danger he’d posed to the city, and had unnecessarily frightened people by talking about whether or not you can catch Ebola from a bowling ball. In any event, Spencer’s virus died inside the Bellevue biocontainment unit and didn’t reach anyone else in New York.

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  In mid-October, the World Health Organization reported that there had been 9,200 cases of Ebola and 4,500 deaths. It was very clear that Ebola was growing explosively. The virus had reached a critical point. Epidemiologists had completely lost track of it in West African cities. Nobody—not doctors, not citizens, knew who had Ebola and who didn’t. Ebola was spreading at a rate comparable to seasonal flu when it arrives in a city. As they projected the growing number of cases into the future, some epidemiologists predicted that there would be millions of Ebola cases within a year. The Ebola treatment centers were overwhelmed.

  In Sierra Leone, the virus was raging in the capital and had spread throughout the country. There had been more than ten thousand cases reported, and the numbers were still climbing.

  And yet something was happening in the Makona Triangle, at ground zero of the virus’s emergence from the ecosystem. There, the number of new Ebola cases was dropping dramatically. By the end of October, there were almost no new cases of Ebola appearing in the Makona Triangle, and not many new cases around Kenema. Gradually at first, and then suddenly, the Makona strain faded and vanished from the cradle of its birth. Something very strange indeed had happened in the Makona Triangle.

  THE CHAIN OF CARE

  October into December 2014

  “At some point, people just got it,” Lina Moses said, months later. The Kissi villagers in the Makona Triangle were the first to understand the truth: Ebola wasn’t a fiction or a plot by foreigners, it was a communicable disease. People in the Makona Triangle learned the signs and symptoms of the disease. They avoided contact with anybody who looked like they might have the disease. They stopped going to funerals. In addition, they began sending their loved ones to the Doctors’ camps. And eventually the same thing happened all over West Africa. “What they came to understand is that they cannot take care of the people they love,” Lina Moses continued. “They have to surrender their infant, their spouse, or their beloved grandmother to an isolation ward in order to save the rest of their household. I think I would have a really hard time doing that in the same situation. When the stakes are your life and the lives of your family members, you figure things out pretty fast.”

  Anja Wolz, the Kailahun camp’s clinical manager, made journeys to Kissi towns and villages in the Triangle during August and September of 2014, at the time when the virus was exploding in the cities. What she saw in the Triangle was that the Kissi villages had started practicing reverse quarantine, closing themselves off from outsiders to prevent the virus from entering the village. This is exactly what villagers did at Yambuku in 1976. “The villagers were quarantining themselves at the local level. Anybody who came into a village was checked beforehand,” Wolz said. “They were checking who was coming into the village, who was sick.” Villagers inspected Wolz and her driver for symptoms and made them wash their hands in chlorine before they were allowed into a village. At one village, Wolz and her driver were told they couldn’t go in at all, because the village had isolated itself from the world. “It was like something out of the past,” Wolz said. “They weren’t going to burials, they stopped kissing each other, they weren’t touching each other. Behavior changes.”

  “This is how all outbreaks end,” Armand Sprecher, the Doctors’ official in Brussels, said. “It’s always a change in behavior. Ebola outbreaks end when people decide they’re going to end.”

  In the cities, people wouldn’t touch or go near any place or person that might have particles. When Ebola appeared in a family, the neighbors would shun the family. If you lived in Wellesley, Massachusetts, and a Level 4 virus was going around town, and somebody on your street was sick at home, you might not want your kids to play with those kids. Africans continued shunning Ebola-affected families even after the virus was gone from the family. People who wandered in the streets looking sick, or who lay on the streets dying, were left to die alone. There was no help for strangers. All across West Africa, people stopped shaking hands, stopped hugging or touching one another, and they went full OCD about washing their hands in bleach water. For a while, people changed their burial practices, too. No sane person wants to kiss an Ebola-ridden corpse.

  The Ebola war wasn’t won with modern medicine. It was a medieval war, and it went down as a brutal engagement between ordinary people and a life form that was trying to use the human body as a means of survival through deep time. In order to win this war against an inhuman enemy, people had to make themselves inhuman. They had to suppress their deepest feelings and instincts, tear down the bonds of love and feeling, isolate themselves from or isolate those they loved the most. Human beings had to become like monsters in order to save their human selves.

  In West Africa there was no tradition similar to the Ancient Rule of the Congo Basin. But in 2014 the rules of the engagement with Ebola were exactly the same as the rules that Dr. Jean-François Ruppol had proposed to the people of Zaire when he stood on the table in the marketplace in 1976. The virus was contagious in the liquid humors of the body. If you could recognize the symptoms, if you didn’t touch the liquids, if you avoided contact with people who had the symptoms, and if you let go of the dead, you could save yourself from infection.

  By early October 2014, Monrovia was getting savaged by Ebola. All the beds in all the Ebola treatment centers were full, and there were simply no beds left for anybody sick with Ebola; people were caring for victims at home. Doctors Without Borders, in desperation, decided to distribute 65,000 Ebola disinfection and protection kits across Monrovia. The kits were simple, cheap, and primitive, and included a plastic bucket, bleach, a surgical gown, a mask, and gloves. Doctors’ staff went around handing out the kits and advising people how and when to use them. A kit could be deployed for handling a dead body, or a caregiver could use it to protect themself while they were caring for a sick person.

  In a town in Liberia, a young woman named Fatu Kekula, who was a nursing student, ended up caring for four of her family members at home when there was no room for them in a hospital—her parents, her sister, and a cousin. She didn’t have any protective gear, so she created a bio-hazmat suit out of plastic garbage bags. She tied garbage bags over her feet and legs, put on rubber boots over the bags, and then put more bags over her boots. She put on a raincoat, a surgical mask, and multiple rubber gloves, and she covered her head with pantyhose and a garbage bag. Dressed this way, Fatu Kekula set up IV lines for her family members, giving them saline solution to keep them from becoming dehydrated. Her parents and sister survived; her cousin died. And she herself remained uninfected. Local medical workers called Fatu Kekula’s measures the Trash Bag Method. All you needed were garbage bags, a raincoat, and no small amount of love and courage. Medical workers taught the Trash Bag Method, or variants of it, to people who couldn’t get to hospitals.

  Slowly at first, then more surely, the number of new Ebola cases began to drop. As the number of new cases dropped, the total number of Ebola particles in the swarm dropped at the same time. The particles weren’t able to jump to fresh hosts, and the swarm began to shrink rather than grow. Trapped in the host they had killed, unable to reach a new host, vast numbers of particles died along with the ruined host. By the end of 2014, Ebola was fading away. In the Makona Trian
gle it was virtually gone.

  Mapp Bio and Kentucky BioProcessing made three batches of pharma-grade ZMapp, and in April 2015, the NIH began a trial of ZMapp in Sierra Leone. By this time there were so few Ebola patients that it was very difficult to get statistics on ZMapp. In any event, the drug was given to eleven patients, and all of them recovered. But then the drug failed to save a boy, who died soon after receiving one dose of the drug. There just wasn’t enough statistical evidence to say for sure that ZMapp is effective against Ebola. The U.S. Food and Drug Administration ruled that ZMapp showed promise but could not be licensed for emergency human use without more testing in animals.

  Can ZMapp actually hammer down Ebola in minutes? The small amount of evidence, so far, suggests that ZMapp can, in fact, cure Ebola disease in some or many people, and that the drug can act extremely rapidly in some people. Antibody drugs have begun to look like a huge advance in medicine. Researchers, including the scientists at Mapp Bio, have been developing more antibody drugs against Ebola and for other viruses. ZMapp may be an example of a class of silver-bullet drugs—angels’ swords—that could cure a person of many kinds of infectious diseases. Someday there could be antibody drugs that can cure infections by viruses, by drug-resistant bacteria, even possibly cure diseases caused by advanced bioweapons. Whether or not ZMapp proves to be a sure-fire Ebola-killer, it had been a huge breakthrough in the war on infectious diseases.

  While Kentucky BioProcessing was rushing to make more ZMapp, there was only one pharmaceutical-grade course of the drug anywhere in the world. This was Course Zero, sitting in a freezer somewhere in the United States. When Course Zero was the only ZMapp in the world, it seemed extremely precious—a national asset.

  At the White House, officials in charge of the security of the President of the United States carefully studied the medical case file on Kent Brantly and Nancy Writebol. “I’ve seen the file,” Gary Kobinger explained later. “When you read it you say, ‘Wow, this really works.’ ” Sometime in the fall of 2014, an official at the White House contacted an official at the National Institutes of Health and asked him if there was any ZMapp available for the White House. The NIH then learned of the existence of Course Zero. Course Zero ended up sitting in a freezer at an undisclosed location in or near Washington, D.C. Course Zero, which might have been used on Lisa Hensley if she’d come down with Ebola, was now reserved for the exclusive use of the President of the United States. Just in case Ebola ever comes to Washington.

  As the Ebola epidemic died down, the NIH started testing the VSV-ZEBOV vaccine for Ebola, and it showed solid effectiveness. At this writing, the vaccine is being tested in eastern Congo, where Ebola virus has broken out and is running wild—and no doubt evolving in human bodies.

  As the tide of the Makona strain receded, it left its dead scattered across eight countries, including Spain and the United States. Thirty thousand people had been infected. More than eleven thousand people had died of the virus, and untold thousands more had died because they couldn’t get medical care during the epidemic, since hospitals were devastated. Seven percent of all the doctors in Sierra Leone were dead. The medical infrastructure of Guinea, Liberia, and Sierra Leone had been wrecked. The three nations’ economies had functionally collapsed. At Kenema Government Hospital, at least thirty-seven nurses were dead. Two Kenema hospital doctors were also dead—Humarr Khan and Sahr Rogers. In the end, the Ancient Rule prevailed, and the emerging virus temporarily went back to its hiding place in the virosphere.

  STONY BROOK, LONG ISLAND, NEW YORK

  About 1:00 p.m., June 1, 2016

  In the spring of 2016—a year after the great Ebola epidemic subsided, a postdoctoral researcher named William “Ted” Diehl began doing experiments with Ebola proteins that had been collected from the different mutant Ebolas that evolved in the swarm as the epidemic went along. Diehl was looking closely at the different kinds of “fish” in the school, as it were, and was working in the lab of a prominent AIDS researcher, Dr. Jeremy Luban, at the University of Massachusetts Medical School.

  Ted Diehl discovered that one of the Ebolas, the one now known as the A82V Makona Variant, or the Makona strain, was four times better able to infect human cells in a test tube than the wild, natural Ebola that got into the little boy in Meliandou. The Makona strain was really hot in human cells. Was there something different about this Ebola? What, exactly, made the Makona so hot?

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  Diehl’s boss, Jeremy Luban, called Pardis Sabeti. He didn’t know anything about the Makona strain other than it seemed very hot. Sabeti got excited. She told him that the Makona strain had taken over in West Africa. It had knocked out all the other Ebolas; it was the Ebola that had swept through the cities of West Africa, the one that had killed Humarr Khan, the one that had gotten to Dallas and New York. Yes, she told Luban, this Ebola was the fish with the sharpest teeth, the real killer in the swarm. And it was different from the other Ebolas by only one letter in its 18,959 letters of code. The change in one letter had caused a slight change in one of the proteins of Ebola.

  Nobody knew what made the Makona strain hot. But on the first of June, 2016, Ted Diehl was in Stony Brook, Long Island, sitting at the dining room table in his wife’s apartment, and drinking green tea. (The couple worked in different places.) He was looking at an image on his laptop of the exact structure of a certain protein that exists in the soft knobs that stud the outside of an Ebola particle. The knobs help an Ebola particle get inside a human cell.

  Proteins are made of long strings of amino acids, which are like necklaces, and the necklaces are folded in special ways. In the case of the hot Ebola, the Makona strain, one amino acid was different in the protein of the soft knob. In the wild Ebola, the Meliandou Ebola, the amino acid was alanine. It got changed to a different amino acid, valine, in the Makona strain. The change seemed insignificant: Why should it make Ebola four times more infective?

  Ted Diehl began rotating the image of the protein on his computer screen, studying its curious shape. All of a sudden, in a flash of insight, he saw that the shape of the protein could fit better on something that sticks out of a human cell membrane. Like a key fitting in a lock. He saw that the mutant Ebola protein could stick to the skin of a human cell better, and could open the cell up, so that the Ebola particle could get inside the cell more easily. The mutant Ebola sticks to a receptor knob on the outside of a human cell that pulls cholesterol into the cell, called the Niemann-Pick receptor. Ebola uses the Niemann-Pick receptor to invade human cells. (Niemann-Pick disease is an inherited, fatal disease in which a person’s cells can’t absorb cholesterol properly. For this reason, a person with Niemann-Pick disease is presumably immune to Ebola.)

  Sitting there at the kitchen table that day, Ted Diehl became the first person to see exactly what gave the Makona strain an edge at invading humans. “It felt like holding a lottery ticket and seeing all the numbers come up,” Diehl says. “Out of dumb luck we scored a huge win.” Diehl had gotten a look into the microscopic halls of nature and had seen a tiny thing that looked different to him. Maybe he had seen how close the world came to something much worse than ten thousand deaths and three nations wrecked.

  At the same time that Ted Diehl was figuring out what made the Makona strain so dangerous, a researcher named Jonathan K. Ball, at the University of Nottingham, in England, and colleagues of his, discovered something equally disturbing about the Makona strain. It didn’t infect bat cells as well, while it infected human cells much better. In other words, the Makona strain is a humanized Ebola. The Makona strain understands people better than does any other kind of Ebola.

  Pardis Sabeti had this to say: “The mutation increased the virus’s ability to infect human cells, while it made the virus less able to infect other animals. As the virus was transmitting from human to human it was improving its ability to do so. We know viruses mutate. Most mutations of a virus don’t do
anything. But if you give the virus enough chances, a match may light, and a spark may go.”

  In other words, if the Makona strain hadn’t been stopped quickly, it would have continued improving its ability to spread in humans. It would have become yet more humanized. The world got lucky this time. If the Makona strain had raced into a poor supercity, it would have gotten into many more thousands of people, and gotten many more chances to evolve and change. For a long time after the Ebola epidemic subsided, nobody really understood just how close the world had come to a much bigger disaster. What might have happened if the Makona strain had blown up in the supercity of Lagos, population twenty million, after Patrick Sawyer brought the virus to the city? If Lagos had gone hot, could the virus have moved to other cities around the world, and could more cities have gone hot? If the Makona strain had kept on evolving, getting to know the human body and the human immune system better and better, the Ancient Rule eventually could have arrived on the streets of Los Angeles, Tokyo, the industrial Ruhr of Germany, the shanties of São Paulo. We are one species, all connected, but we are just one thing to a virus: a host.

  What would it be like if a Level 4 virus event occurred and the Ancient Rule arrived in the supercity of New York? It wouldn’t take much to produce the Ancient Rule in New York City. A dry virus with high mortality that infects people through the lungs. No vaccine, no medical treatment for the virus. If you take the subway, if you ride in an elevator, you can be infected, too. If the Ancient Rule came to New York City, we can imagine people lying facedown on the street or in Central Park, crowds staring and hanging back. People begging for help, no one willing to help. Police officers wearing full PPE gear. People needing ambulances. No ambulances. Hospitals gone medieval. Medical staff absent, dying, overwhelmed. All hospital beds full. People being turned away on the street from Bellevue Hospital. Medical examiner facilities gone hot as hell and crammed with corpses. Nobody in their right mind would enter a New York City hospital during a time of the Ancient Rule. Transportation frozen. Food supplies dwindling or absent. Schools closed. People avoiding supermarkets for fear of contagion. Prophets and visioners predicting the future and offering cures. People leaving the city, bringing the virus with them. Airports infective, flights canceled. Parents giving care to their sick children in apartments, at home. If someone in a family got sick, there would have to be one designated caregiver, a person willing to sacrifice their life in an attempt to give care to a loved one. Wealthy people spending money like water trying to save themselves; the poor and disadvantaged, as always, bearing the worst of it. If there is a vaccine or drug that can help, there will be corruption. Companies and individuals hoarding vaccine, selling it at sky-high prices.