As the number of COVID-19 cases in the United States streaks toward 5 million, it may surprise you to learn that 80% of those who test positive for the disease never infect anyone else with the virus.
Instead, new research suggests the disease weaves its way, rapidly, into the population because of a confluence of events. They are largely driven by contact with people who happen, briefly, to be highly contagious in the wrong place, at the wrong time.
It is a phenomenon known as super-spreading, and experts at Seattle’s Fred Hutchinson Cancer Research Center are using complex computer simulations of viral transmission among individuals to gain a better understanding of how this virus, SARS-CoV-2, with an unknowing assist from super-spreaders, manages to wreak so much havoc in populations.
In research newly posted in medRxiv, a team led by Fred Hutch postdoctoral scientist Dr. Ashish Goyal, infectious diseases physician Dr. Joshua T. Schiffer and epidemiologist Dr. Bryan T. Mayer reports some surprising insights using a computer model that compares the behavior of COVID-19 with influenza.
While existing data shows that people who are infected with SARS-CoV-2 may shed tiny amounts of the virus for weeks, the model suggests that they usually only shed enough to be contagious for a brief period — likely only one or two days.
— Dr. Joshua T. Schiffer
On the other hand, the model suggests that for many, but not all infected people, the two-day contagious period may have ended before a COVID-19 patient comes down with symptoms, and that before then, the person may already have spread the virus to dozens of others.
Schiffer emphasized that the model cannot rule out the possibility that a small minority of infected people may be contagious for an extended period during the symptomatic phase of illness.
“The ethical thing to do as an individual is to walk around with the assumption that you’re infectious and contagious, and that it’s your responsibility to protect the public. That doesn’t change at all,” he said.
MedRxiv is a “preprint server,” an online journal that presents research for discussion prior to receiving peer review — the time-consuming professional critiques that are being bypassed due to the urgency of COVID-19. As such, Schiffer stresses that his research is preliminary and subject to revision, but important enough to be presented to colleagues in the field for their consideration.
The team’s model indicates that both influenza and COVID-19 share this brief contagious period in common. Yet SARS-CoV-2 may be more prone to super-spreading, their research suggests, because of airborne transmission, which makes it much more dangerous in crowded, confined spaces.
The six-foot rule for social distancing springs from evidence that COVID-19 spreads in droplets that can travel only short distances before settling to the ground. Airborne transmission envisions the virus can be carried in tinier particles of moisture that hang in the air longer and can drift across a room.
Suspicions that COVID-19 spreads through airborne transmission remain controversial even after the World Health Organization reluctantly acknowledged last month there was some evidence of it.
To gain a better understanding of COVID-19’s spread, the team built their computer model to simulate the transmission patterns of viruses, based on similar methods that Mayer and Schiffer have used to track the behavior of several herpesviruses. The goal was to simulate the infectious behavior of COVID-19 using thousands of scenarios based on different assumptions about factors that might influence transmission.
Among those assumptions were:
After loading different numbers for these and other variables into their computers, the researchers ran approximately half a million simulations that — using the magic of computer algorithms — spat out thousands of predicted courses of infection. Think of them like strands of spaghetti tracking across a chart.
Next, they plotted the course of actual transmissions based on epidemiological data — more spaghetti — and found that only a few of the simulated scenarios matched that of the real-world data. At that point, the researchers could infer which of their assumptions about the virus were likely to be correct.
The scientists also ran transmission scenarios for influenza and found some similarities and some differences that have implications for understanding how to prevent this new disease.
“Let’s say you have two people walk into a crowded, closed room, with poor ventilation,” Schiffer explained, “and one of those people has influenza, and one has SARS-CoV-2. Both are unfortunately shedding at the highest viral load possible. Our model shows the person with influenza will likely expose far fewer people to their virus within that crowded environment than the person with SARS-CoV-2.
“That’s what drives the results in our model. And to me, the most likely explanation for that would be a predisposition towards aerosolization — meaning the virus is physically dispersed over a larger area and perhaps for a longer duration of time with SARS-CoV-2 than with influenza.”
Another inference from the model: “Super-spreader events come from when people are shedding virus at their peak,” Schiffer said. That underscores the importance of knowing, if possible, how soon after exposure a person might reach their two-day window of contagiousness. In other words, most people who are infected with SARS-CoV-2 do not infect anybody, but many people have the potential to be super-spreaders.
“They have to show up in a crowded place, and they have to do so when they are shedding at a high viral load,” he said.
Dr. Dan Reeves, a research associate in Schiffer’s lab and co-author of the paper, said that there are some potentially reassuring findings from the computer simulations. One is that contagiousness lasts only a couple of days, so repeat testing after a positive result may not be necessary. Also, any early treatment that can reduce the viral load (the amount of virus measured from a swab sample) might have “an outsized impact on transmission reduction.”
Finally, said Reeves, because masks can help reduce the amount of virus, even slightly, during an exposure, “wearing a mask really will help!”
Sabin Russell is a staff writer at Fred Hutchinson Cancer Research Center. For two decades he covered medical science, global health and health care economics for the San Francisco Chronicle, and wrote extensively about infectious diseases, including HIV/AIDS. He was a Knight Science Journalism Fellow at MIT, and a freelance writer for the New York Times and Health Affairs. Reach him at firstname.lastname@example.org.
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