“I’m fine” were the first words out of Henry’s mouth. Jill immediately teared up when she heard his voice, even though it was five in the morning in Atlanta. “They just now gave me my satellite phone or I would have called you sooner.”
“Where are you?”
“I’m in a tent by myself. There are medical teams arriving from all over the place. They’ll be up and running in a matter of hours.”
“How long do you have to stay in quarantine?”
“Fourteen days, as long as there are no symptoms.”
“Well, are there any?”
“No, and don’t worry.”
“You must be going crazy.”
“I’m berserk. I should be leading the team, but instead I’m in this little tent with a cot and a camp chair.”
Jill laughed at the image, only because she was so relieved, but the thought of Henry having to hold still, alone, in the middle of a major health crisis was wrenching. “If it weren’t for you, they wouldn’t be there at all,” she reminded him.
“Tell the kids how much I love them,” he said. “And that I’ll be home as soon as I can.”
He called Maria and dictated the team he wanted her to assemble. “I need Marco to head it,” he said, referring to Marco Perella, who had been with him through many disease campaigns. Smart, ironic, reliable, he had started as an officer in the Epidemic Intelligence Service in Henry’s lab at the CDC and was now his number two.
“He’s already in the air,” she said.
“And we’ll need something more than a basic field lab.”
“I’ve taken care of that,” she said.
“You’re working fast,” Henry said appreciatively.
“I just made a list all the things I knew you were going to demand and started checking them off.”
“You know me too well,” he said. “Listen, Maria, the Indonesian authorities have to be made to see the seriousness of this event. It’s unlikely we’ll be able to confine this outbreak to the camp. We need to run down everyone who has been in or out of this place in the last month. Food services, military, medical personnel—every single person.”
“Henry! I’m on it!” Maria exclaimed.
“I’m sorry, I know you are. There’s nobody better. I’m just frustrated at being sidelined.”
“You’re not sidelined. We’re depending on you. I’ll be in touch every day.”
Before he rang off, Henry said how sorry he was that Maria had lost a friend in the Rome attack.
“Ah, yes, thanks, Henry. We grew up together. She was my best friend from childhood. It’s terrible for her family.”
“I’m sure it’s hard for you as well.”
“You know what is really hard,” Maria said, her voice cracking. “The hatred I feel for the people who did this. They don’t care how precious are the lives they take. They only want to kill and draw attention to their own grievances. Maybe unconsciously they just want us to feel the way they do. And now I do. I’ve worked my whole life for health and for peace and now I’m full of rage. I can’t stand what they did to my friend—and I despise the person they have made me become.”
Marco called moments later, from the plane. He was bringing a dozen top researchers from Atlanta. They would join with the WHO team and others who were already on the ground. Marco and Henry went through a familiar process of eliminating possible pathogens to concentrate on the most likely causes of an illness but, at the same time, making sure that they weren’t ignoring less obvious candidates.
“Cyanosis,” Marco said, pointing to the most distinctive symptom. “Do you think poison?”
Henry considered. There were cases of women dying after swallowing nitrobenzene to induce an abortion. They turned blue. Printers had been known to commit suicide by drinking India ink. Some heavy metals, such as cadmium, caused cyanosis, but the level of exposure would have to be extraordinary.
“What about rat poison?” Marco said. “That could account for the bleeding.”
The camp was beset with rodents. Most such poisons were blood thinners, however, and the blood sample that Henry had extracted from the doctor’s corpse was densely coagulated. If rats were carrying the disease, it could be spread by their ticks or fleas, like bubonic plague. If the plague bacterium, Yersinia pestis, got into the lungs, it became transmissible between humans, highly contagious, and almost impossible to treat. Lethality was nearly 100 percent.
Henry’s mind was always stalked by the fear that some form of the plague would recur. At Hopkins, he had taken a course in the history of medicine and was fascinated by the plague bacterium. His professor drew a graph on the chalk board of the estimated human population over time. The chart showed steady growth until the sixth century, during the reign of the Roman emperor Justinian, when fifty million people died—about a quarter of the entire world population. The next plague pandemic was the deadliest outbreak in human history. Known as “the Black Death” because of the gangrene that appeared on the extremities of the infected person, it began in China in 1334 and followed the trade routes through Central Asia and Europe, killing as many as 200 million people before subsiding in 1353. The last plague pandemic also began in China, in the mid-nineteenth century, and, thanks to steamships, quickly spread around the world. India alone lost 20 million people, and nearly 80 percent of those who contracted the disease died of it. There was still no effective vaccine for pneumonic plague.
Henry had already gotten several flea bites in his quarantine tent. He had not seen the characteristic swollen lesions of plague on the bodies in Kongoli, however. “It’s still possible that it is spread by rats,” said Henry, “although according to Dr. Champey’s notes, the disease spread slowly at first, then went rapaciously through the camp, following the pattern of an infectious disease.”
“Have you got a median age of death?” Marco asked.
“They’re working on the latest count,” said Henry. “Most of the mortality is among young men, but of course the population of the camp is entirely male and skews young. Another thing to consider is that the reason the MSF doctors came in the first place was to treat the HIV infection, so presumably a significant percentage of the detainee population have compromised immune systems. That could make the disease somewhat less fearsome if it escapes into the general population.”
“But one assumes that the doctors themselves did not have HIV, and they also died,” said Marco.
“Yes, and rather quickly,” Henry agreed. “We could be dealing with a disease that is not normally found in humans, but because of the lowered immune response the disease took hold and adapted to the human host.”
“Means of transmission?” asked Marco. “Mosquitos, possibly? A bacterium in the water?”
“It moves too quickly for mosquitos,” said Henry. “We’ll see if the spread halts when your team takes control of the food and water sources, but it doesn’t have the characteristics of any bacterium I know of. I put my money on a virus.”
“The suddenness of the onset does suggest that. The high lethality, the rapid spread, the hemorrhagic fever—yes, it could be Ebola. But the only strain of the Ebola virus known to be in Asia is Reston virus, and that’s not been known to be pathogenic in humans.”
“What about Lassa fever or Marburg?”
“The carriers for those diseases are African mice and Egyptian fruit bats. Not found in Indonesia.”
“So, it’s a puzzle,” said Marco.
“A considerable puzzle,” Henry agreed.
“Stay well, Henry,” Marco said as he signed off. “We’re going to need you on this one.”
HENRY HAD COME to virology late in his career. His early work was in highly pathogenic bacteria, the source of many formidable diseases. Pneumonia, history’s great killer. Plague, the word itself evoking terror. Tuberculosis, still the number one cause of death from infectious disease. Yes, Henry respected bacteria. He thought he understood the clever mechanisms of contagion. Then Ebola had taken him to school. Among diseases, it was a diva—dramatic, sudden, and vicious. Bleeding was the most obvious symptom, out of every pore, eyes, ears, nose, anus, even the nipples, the fluid being a pathway for the virus to escape the body and search out new victims. At first, doctors mistook Ebola for Lassa fever, but one of the defining symptoms of Ebola was hiccups. No one knew why. Like influenza and the common cold, Ebola’s genetic material was composed of ribonucleic acid, or RNA. Other viruses, such as smallpox and herpes, were formed from DNA, deoxyribonucleic acid. The singular character of RNA viruses was that they were constantly reinventing themselves over and over again in what was called a “mutant swarm.”
Ebola was no more than a strand of RNA, coated in protein and wrapped in a lipid envelope. It sometimes developed branching arms or tied itself into a loose knot, like an ampersand or a treble clef. It was transmissible to humans from certain animals in the wild, especially bats and monkeys. It spent as much as three weeks in the body before symptoms showed up, so a full-blown epidemic could be undetectable until it suddenly fell like a guillotine blade. If the virus was left untreated, the mortality rate approached 90 percent, although intensive palliative care could cut that figure in half. Unlike influenza or measles, Ebola was not airborne. It only spread through contact with bodily fluids—sex, kissing, touching, and, especially, caring for the sick and the dead. It was a disease that specifically targeted love and compassion.
The singular figure who shaped Henry’s approach to epidemiology was his first boss at the CDC, Dr. Pierre Rollin, a Frenchman with merry eyes, who was chief of the Viral Special Pathogens Branch. Henry watched him give what Pierre called Ebola 101 in a mosque in Guinea during the 2014 outbreak. Imams from all over the country came. Ebola was a terrifying new phenomenon, but Pierre’s clarity and easy manner did much to calm the panic, which can be more contagious than the disease. Once, in a distant field hospital, Pierre and his team were trying to help a deeply suspicious community contain the outbreak. Family members felt obligated to wash the bodies of their loved ones, although the corpses were still shedding the virus. After a young boy passed away, his parents demanded his body, which would almost certainly kill them and many others. Tensions were at a flash point when Pierre, then in his sixties, took a shovel and dug the grave himself. This show of humanity and compassion was a model Henry aspired to emulate.
Once Henry decided to devote his career to the study of viruses, he was daunted by the volume and diversity of the viral world, and shocked by the absence of scientific understanding. Twenty years before, no one thought there were viruses in the oceans, but researchers had since shown that a single liter of seawater contained about 100 billion of them. Curtis Suttle, a marine virologist at the University of British Columbia, collected seawater from oceans all over the world and found that 90 percent of the viruses he examined were totally unknown to man. Yet every virus carried the genetic codes for proteins—meaning that each one had a mission. What that mission was remained a mystery.
In 2018, Suttle and other scientists looked on mountain peaks for evidence of viruses in the free troposphere, the concourse of jet travel just below the stratosphere. They were seeking an answer to a puzzle about the occurrence of nearly identical viruses in widely separated parts of the planet and vastly different environments. Was it possible that viruses—say, in dust or sea spray—could be swept into the atmosphere and transported from one continent to another? The scientists placed buckets on mountaintops in Spain’s Sierra Nevada, nine thousand feet high, and waited to see if viruses would rain into them. They were stunned by what they found. According to their calculations, more than 800 million viruses were deposited every day on every single meter of the earth’s surface. Most of these viruses preyed on bacteria, not humans. The total number of viruses on the planet was estimated to be a hundred million times more than the number of stars in the universe.
When a virus infected a cell, it inserted its own genes, and then used the energy of the cell for reproduction—in effect, turning the victimized cell into a virus factory. Once under the genetic command of the virus, the cell might be ordered to produce new viruses until it burst open and died, releasing sometimes thousands or even tens of thousands of new viral particles into the host organism to invade new cells. Alternatively, the virus and the cell might learn to coexist, as was the case with herpes, and the infection would last indefinitely.
For Henry, the most surprising feature of viruses was that they were a guiding force behind evolution. If the infected organism survived, it sometimes retained a portion of the viral material in its own genome. The legacy of ancient infections might be found in as much as 8 percent of the human genome, including the genes that controlled memory formation, the immune system, and cognitive development. We wouldn’t be who we are without them.