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At a birthday party in Texas in May, one man reportedly infected 17 members of his family with the coronavirus.

Reading reports like these, you might think of the virus as a wildfire, instantly setting off epidemics wherever it goes. But other reports tell another story altogether.

In Italy, for example, scientists looked at stored samples of wastewater for the earliest trace of the virus. Last week they reported that the virus was in Turin and Milan as early as Dec. 18. But two months would pass before northern Italy’s hospitals began filling with victims of COVID-19. So those December viruses seem to have petered out.

As strange as it may seem, these reports don’t contradict each other. Most infected people don’t pass on the coronavirus to someone else. But a small number pass it on to many others in so-called superspreading events.

“You can think about throwing a match at kindling,” said Ben Althouse, principal research scientist at the Institute for Disease Modeling in Bellevue, Wash. “You throw one match, it may not light the kindling. You throw another match, it may not light the kindling. But then one match hits in the right spot, and all of a sudden the fire goes up.”

Understanding why some matches start fires while many do not will be crucial to curbing the pandemic, scientists say. “Otherwise, you’re in the position where you’re always one step behind the virus,” said Adam Kucharski, an epidemiologist at the London School of Hygiene and Tropical Medicine.

In some diseases, such as influenza and smallpox, a large fraction of infected people pass on the pathogen to a few more. These diseases tend to grow steadily and slowly. “Flu can really plod along,” said Kristin Nelson, an assistant professor at Emory University.

But other diseases, like measles and severe acute respiratory syndrome, or SARS, are prone to sudden flares, with only a few infected people spreading the disease.

Epidemiologists capture the difference between the flare-ups and the plodding with something known as the dispersion parameter. It is a measure of how much variation there is from person to person in transmitting a pathogen.

But James Lloyd-Smith, a UCLA disease ecologist who developed the dispersion parameter 15 years ago, cautioned that just because scientists can measure it doesn’t mean they understand why some diseases have more superspreading than others. “We just understand the bits of it,” he said.

When COVID-19 broke out, Kucharski and his colleagues tried to calculate that number by comparing cases in different countries.

If COVID-19 was like the flu, you’d expect the outbreaks in different places to be mostly the same size. But Kucharski and his colleagues found a wide variation. The best way to explain this pattern, they found, was that 10% of infected people were responsible for 80% of new infections.

Kucharski and his colleagues published their study in April as a preprint, a report that has not been reviewed by other scientists and published in a scientific journal. Other epidemiologists have calculated the dispersion parameter with other methods, ending up with similar estimates.

Now researchers are trying to figure out why so few people spread the virus to so many.

Many countries and states have fought outbreaks with lockdowns, which have managed to draw down COVID-19’s spread. But as governments move toward reopening, they shouldn’t get complacent and forget the virus’ potential for superspreading.

On the other hand, knowing that COVID-19 is a superspreading pandemic could be a good thing. Since most transmission happens only in a small number of similar situations, it may be possible to come up with smart strategies to stop them from happening.

“By curbing the activities in quite a small proportion of our life, we could actually reduce most of the risk,” Kucharski said.