him along the side of the basin amid a fusillade of stones. He thought he might be screaming, but the roar was too loud for him to hear his own voice. He was no longer touching the ground. The crush lifted him out of his sandals. He prayed to be saved. He prayed to be alone and untouched. There was no air anywhere; he prayed for breath. Then a gap opened in the crowd as they slipped past the edge of the basin and Bambang fell to the ground, thanking God for his deliverance as worshippers helplessly trod upon his body.
11
What Do We Have Here?
While Henry waited in the tent overlooking Mecca for Majid and Colonel al-Shehri to return from the holy city, he joined a conference call with Maria Savona in Geneva, Catherine Lord, the chief medical officer at CDC in Atlanta, and Marco Perella, who was still in the Kongoli camp in Indonesia. Marco had good news: amazingly, other than the dead gravedigger, there were no reported cases in Jakarta.
Catherine Lord took over from there. “It’s something in the Orthomyxoviridae family. Probably influenza, but we’ve compared it against thousands of virus sequences in the database, and so far we haven’t been able to find an identical match.”
Like so many dangerous things in nature, influenza viruses were beautiful, covered with protein spikes called hemagglutinin (H) and neuraminidase (N), which functioned like a pirate boarding party. The hemagglutinin fastened onto a cell like a grappling hook and plunged viral particles into the cell. Once inside, the virus used the cell’s energy to replicate itself thousands of times. As the newly hatched viruses budded from the cell, the neuraminidase protein cut them loose. Within a few hours of exposure, the victim became infectious, releasing half a million virus particles into the air with every cough or sneeze. The particles floated into the lungs of people nearby, or landed on surfaces, where they could survive for hours at a time. Influenza had many strategies for propagation, but the most insidious was its ability to mutate, constantly reinventing itself, slipping past the body’s attempts to create immunity and science’s efforts to make effective vaccines.
Influenza viruses fell into four distinct groups. By far the most common and the most virulent in humans were influenzas A and B. In the Kongoli cases, influenza A was the most likely category, because it was typically more virulent than influenza B. There were eighteen hemagglutinin and eleven neuraminidase subtypes in influenza A viruses that had been discovered so far, but only H1, 2, and 3, and N1 and 2, typically caused seasonal human influenza. The highly infectious 1968 Hong Kong flu, for instance, was an H3N2 virus. Influenza B viruses were found only in humans, and could also be severe, but they did not cause pandemics like A viruses did. There were two other influenzas, C and D, which differed from A and B by not having the neuraminidase protein. Influenza C was common in humans, especially in infants, but rarely life-threatening. Influenza D was usually found in cattle, with occasional cases found in humans and domestic pigs.
“Also, we can’t seem to get this damn Kongoli to grow,” Catherine continued. “We’ve used chick embryo fibroblasts, MDCKs, Vero cells from African green monkeys, bats, and baby hamster kidneys, but none of the standard cell lines work with this stuff.”
“Where does it stand now?” Henry asked.
“We’re just starting to test it in ferrets and chickens,” said Catherine. “It’s a mystery bug.”
“Maria, are there any other outbreaks that resemble Kongoli?” Henry asked.
“We’ve got seasonal influenzas circulating, both A and B, but they are historic strains, nothing novel. So far it’s been a moderate year.”
The conversation was tense and urgent, but also puzzled and frustrating. Everyone understood the stakes. They were facing what could be the most catastrophic pandemic of their lifetime. It had to be contained, and fortunately, with the exception of the gravedigger, it seemed to be. Unlike during the 2018 Ebola outbreak in the Democratic Republic of the Congo, where international health workers were murdered by armed militias, in Indonesia workers were protected by government forces. The Indonesian authorities were doing their job. If they could keep the disease bottled up in the Kongoli camp while researchers figured out exactly what it was, the NIH and pharmaceutical companies would work to develop a vaccine. With luck, humanity might slip past this mortal threat. The stray pilgrim in Mecca was worrisome, but he was an outlier. There was nothing to