by his stutter, which sometimes brought him to what seemed an impassable halt; but Sophiano pushed on, and between blockages his words came quickly.
He had been traveling to one of the gold camps. Farther upriver. And stopped in Mayibout 2 to stay with family. That night one of his nieces said she was feeling bad. Malaria, everyone thought. A routine thing. The next morning, it got worse. Then other people too. They vomited, they had diarrhea. Started dying. I lost six, Sophiano said. Thony had gotten the number right but was a little confused about the identities. An uncle, a brother, a widowed sister-in-law. Her three daughters. The men in white suits, they came to take charge. One of them, a Zairian, had seen the disease before. At Kikwit. Twenty doctors had died there at Kikwit, the Zairian told us. They told us, this thing is very infectious. If a fly lands on you after having touched one of the corpses, they said, you will die. But I held one of my nieces in my arms. She had a tube in her wrist, an IV drip. It got clogged, backed up. Her hand swelled. And then with a pop her blood sprayed all over my chest, Sophiano said. But I didn’t get sick. You’ve got to take the remedy, the doctors told me. You’ve got to stay here twenty-one days under quarantine. I thought, the hell with that. I didn’t take the remedy. After my family people had been buried, I left Mayibout 2. I went to Libreville and stayed with another sister, hiding, Sophiano confessed. Because I was afraid the doctors would hassle me, he said.
This was our last evening in the forest before a resupply rendezvous four or five miles onward, at a point where Fay’s preplotted line of march crossed a road. That road led eastward to Makokou. Some of Fay’s crew would leave him there. They were exhausted, spent, fed up. Others would stay with him because, though also exhausted, they needed the work badly, or because it was better than gold mining, or because those reasons supplemented another: the sheer fascination of being involved with an enterprise so sublimely crazed and challenging. Another half year of hard walking across forests and swamps lay between them and Fay’s end point, the Atlantic Ocean.
Sophiano would stay. He had been through worse.
20
The identity of Ebola’s reservoir host (or hosts) remains unknown, as of this writing, although suspects have been implicated. Several different groups of researchers have explored the question. The most authoritative, most advantageously placed, and most persistent of them is the team led by Eric M. Leroy, of CIRMF, in Franceville, Gabon. As mentioned earlier, Leroy was one of the visiting doctors dressed in mystifying white suits who took part in the response effort at Mayibout 2. Although he and his colleagues may not have saved many (or any, as remembered by Thony M’Both) of the Mayibout patients from death, that outbreak was transformative for Leroy himself. He trained as an immunologist as well as a veterinarian and a virologist, and until 1996 studied the effects of another kind of virus (SIV, of which much more below) on the immune systems of mandrills. Mandrills are large, baboonlike monkeys with red noses, puffy blue facial ridges, and contorted expressions, all of which give them the look of angry, dark clowns. Leroy was also curious about the immune physiology of bats. Then came Mayibout 2 and Ebola.
“It is a little bit like a fate,” Leroy told me when I visited him in Franceville.
Back at CIRMF after Mayibout 2, he explored Ebola further in his lab. He and a colleague, like him an immunologist, investigated some molecular signals in blood specimens taken during the outbreak. They found evidence suggesting that the medical outcome for an individual patient—to survive and recover, or to die—might be related not to the size of the infectious dose of Ebola virus but to whether the patient’s blood cells produced antibodies promptly in response to infection. If they didn’t, why not? Was it because the virus itself somehow quickly decommissioned their immune systems, interrupting the normal sequence of molecular interactions involved in antibody production? Does the virus kill people (as is now widely supposed) by creating immune dysfunction before overwhelming them with viral replication, which then inflicts further devastating effects? Leroy and his immunologist colleague, with a group of additional coauthors, published this study in 1999, after which he became interested in other dimensions of Ebola: