Alan Sipress - The Fatal Strain

He approached the traders. He explained that he and his team were looking to take a few samples from the animals: a throat swab, a rectal swab, and some blood. To get the blood, he would have to jab a needle into the heart of each beast. It would be too hard to find a vein through all the fur.

The dealers wanted no part of it. They were afraid Guan might kill or otherwise harm their lucrative creatures, perhaps somehow rob them of that raw bestial energy that made them so coveted by customers. But if Guan was willing to buy the animals, well, then they could do a deal.

Guan pulled a thick wad of Chinese banknotes from his pocket. He had thousands of dollars worth. Yes, he’d pay, he told them. But not full price. Here’s how it was going to be: He would give them one hundred yuan to sample an animal, about twelve dollars each. If the animal died within a day, the trader could notify Shenzhen’s disease-control officers and be compensated in full. The traders agreed and crowded around, eager for easy money.

There wasn’t enough space at each stall to take specimens, and it was too dark to see. In any case, Guan didn’t want to scare off anyone’s business. So once he made his selection, he had the merchants lug the cages to the muddy alley outside. There, amid all the hustle, among the army of porters hauling crates of poultry and produce, exotic roots, mushrooms, and broad bushy vegetables, in between the handcarts, trolleys, and bicycles stacked with boxes, Guan spread a plastic tarp, put down his gear, and prepared to operate. He slipped on a white lab coat and mask. He donned thick protective gloves. The curious quickly crowded around. Guan and his colleagues asked the security guards to push them back. “There’s virus,” he warned.

Before they could begin, Guan’s team had to anesthetize each animal, pump it full of ketamine. That meant coaxing an often hostile creature out of its cage and plunging a needle into its flesh. “It’s very, very dangerous,” Guan advised. “They can bite you. The civet, his head can spin around 360 degrees and you never expect it. To catch it by its back, it’s too hard to do that.” Some beasts cowered, some lunged. So to restrain them, the researchers used a special tool fashioned from a long tube with a Y-shaped attachment that fit around the animal’s neck. With its head thus pinned down, Guan and his colleagues wrestled the critter to the ground and injected the anesthesia.

The subject soon went limp. Guan stuck a needle into its heart, filling a vial with blood. “My medical training helped me a lot,” he recalled. Next he inserted a swab into the animal’s throat and finally into its anus. Over the course of two days, he jabbed and swabbed twenty-five animals, including a half-dozen civets and assorted beavers, hog and ferret badgers, muntjacs, raccoon dogs, and domestic cats.

Back at the university lab, he quickly found the evidence he was looking for. He isolated the SARS Coronavirus in samples from the civets and one raccoon dog. These animals plus a ferret badger had antibodies that indicated they had been infected. There was no way to know whether these species were the ultimate origin of the pathogen or had caught it somewhere else. But it was now clear how the virus was spreading to people. The wild-game markets had to be shuttered.

Based on Guan’s research, WHO urged China to close them down. This time, at least for a while, China listened. New infections ceased.

On July 5, 2003, the world officially defeated what Shigeru Omi, WHO’s regional director for East Asia, later called “the first emerging disease of the age of globalization.” The agency reported that the SARS epidemic was over. The last chain of transmission had been severed in Taiwan, with no new cases detected there since mid-June. The global death toll had been kept below eight hundred.

This epidemic had been contained, first and foremost, through the successful isolation of those infected. Some countries, like Vietnam and Singapore, had tackled it more aggressively than others, adopting measures like temperature screening for airplane passengers and hospital visitors, isolation rooms at airports, designated wards for suspected cases, and rapid tracing of those who’d been exposed. But in the end, the key everywhere was preempting the virus before it could infect again.

Had the pathogen been a novel strain of flu, the strategy would have failed.

Pandemic would have followed, potentially with millions of deaths, and not because of any human miscue. The difference is wired into the biology of these two viruses.

On many scores, there is an uncanny resemblance between influenza and SARS. They are both cruel respiratory afflictions that originate in animals and cross to the humans who prey on them. Like SARS, flu has often if not always emerged out of southern China, where live markets have proven central in amplifying and spreading the disease. Yet flu is far more sinister.

Flu, for starters, is a more nimble virus that spreads with an ease unmatched by other respiratory diseases. “Flu replicates far more efficiently in humans than SARS,” Guan reminded me. “After adapting to humans, SARS can spread quite quickly. But if compared to flu, it is still quite slow.”

In analyzing outbreaks, researchers focus on what they call the basic reproductive number. That figure represents how many other people are typically infected by each sick person. Obviously, the higher the number, the more infectious the disease. An early study of SARS concluded that its reproductive number was lower than that for other respiratory viruses. Researchers said this accounted for why SARS could be contained. Later research compared SARS and flu and found that the transmissibility of flu, as represented by its reproductive number, might be three times greater or more.

SARS was also a soft target because its victims became contagious only after developing a fever and other symptoms. An analysis of SARS patients in Hong Kong found the amount of virus in their nose and throat remained low for the first five days after they started feeling sick, only peaking on the tenth day. When researchers looked at the actual pattern of cases, they reached a similar conclusion that people were rarely contagious in the first few days after they came down with symptoms. Typically it took almost a week or more. For public health authorities, this pattern was a blessing. It gave them ample chance to identify and isolate victims before they disseminated the virus further.

“It is difficult to escape the conclusion that the world was very lucky this time,” wrote a team of researchers from Britain and Hong Kong, adding that an anticipated flu pandemic by contrast could have a “devastating impact.”

With flu, people may be contagious even before they develop symptoms. One analysis estimated that between 30 and 50 percent of those infected with a novel flu strain would catch it from someone who wasn’t yet ostensibly sick. The true figures will depend on the specifics of the strain. But still, in a brewing flu epidemic, there may be no sure-fire way to determine who is contagious and isolate them. Even those infected might be ignorant of their fateful role in spreading the plague until it’s too late.

“Once adapted to human-to-human transmission, influenza is highly transmissible, both in the late incubation period as well as early in the disease. Therefore, its spread may not be amenable to interruption with the same public health measures used to contain SARS,” wrote Peiris and Guan in the cautious language of scholarly publication.

In person, Guan was more succinct: “From a single spark, you can burn up the world.”

I visited Guan several times in the years after SARS. When I last met him at his university office, he was agitated as usual. It was flu, not SARS, that was keeping him up late at night.