No One Really Knows How Much COVID Is Silently Spreading … Again
More immunity and relaxed behavior add up to a new COVID mystery: How common is symptomless spread now?
In the early days of the pandemic, one of the scariest and most surprising features of SARS-CoV-2 was its stealth. Initially assumed to transmit only from people who were actively sick—as its predecessor SARS-CoV did—the new coronavirus turned out to be a silent spreader, also spewing from the airways of people who were feeling just fine. After months of insisting that only the symptomatic had to mask, test, and isolate, officials scrambled to retool their guidance; singing, talking, laughing, even breathing in tight quarters were abruptly categorized as threats.
Three years later, the coronavirus is still silently spreading—but the fear of its covertness again seems gone. Enthusiasm for masking and testing has plummeted; isolation recommendations have been pared down, and may soon entirely disappear. “We’re just not communicating about asymptomatic transmission anymore,” says Saskia Popescu, an infectious-disease epidemiologist and infection-prevention expert at George Mason University. “People think, What’s the point? I feel fine.”
Although the concern over asymptomatic spread has dissipated, the threat itself has not. And even as our worries over the virus continue to shrink and be shunted aside, the virus—and the way it moves between us—is continuing to change. Which means that our best ideas for stopping its spread aren’t just getting forgotten; they’re going obsolete.
When SARS-CoV-2 was new to the world and hardly anyone had immunity, symptomless spread probably accounted for most of the virus’s spread—at least 50 percent or so, says Meagan Fitzpatrick, an infectious-disease transmission modeler at the University of Maryland’s School of Medicine. People wouldn’t start feeling sick until four, five, or six days, on average, after being infected. In the interim, the virus would be xeroxing itself at high speed in their airway, reaching potentially infectious levels a day or two before symptoms started. Silently infected people weren’t sneezing and coughing—symptoms that propel the virus more forcefully outward, increasing transmission efficiency. But at a time when tests were still scarce and slow to deliver results, not knowing they had the virus made them dangerous all the same. Precautionary tests were still scarce, or very slow to deliver results. So symptomless transmission became a norm, as did epic superspreading events.
Now, though, tests are more abundant, presymptomatic spread is a better-known danger, and repeated rounds of vaccination and infection have left behind layers of immunity. That protection, in particular, has slashed the severity and duration of acute symptoms, lowering the risk that people will end up in hospitals or morgues; it may even be chipping away at long COVID. At the same time, though, the addition of immunity has made the dynamics of symptomless transmission much more complex.
On an individual basis, at least, silent spread could be happening less often than it did before. One possible reason is that symptoms are now igniting sooner in people’s bodies, just three or so days, on average, after infection—a shift that roughly coincided with the rise of the first Omicron variant and could be a quirk of the virus itself. But Aubree Gordon, an infectious-disease epidemiologist at the University of Michigan, told me that faster-arriving sicknesses are probably being driven in part by speedier immune responses, primed by past exposures. That means that illness might now coincide with or even precede the peak of contagiousness, shortening the average period in which people spread the virus before they feel sick. In that one very specific sense, COVID could now be a touch more flulike. Presymptomatic transmission of the flu does seem to happen on occasion, says Seema Lakdawala, a virologist at Emory University. But in general, “people tend not to hit their highest viral levels until after they develop symptoms,” Gordon told me.
Coupled with more population-level immunity, this arrangement could be working in our favor. People might be less likely to pass the virus unwittingly to others. And thanks to the defenses we’ve collectively built up, the pathogen itself is also having more trouble exiting infected bodies and infiltrating new ones. That’s almost certainly part of the reason that this winter hasn’t been quite as bad as past ones have, COVID-wise, says Maia Majumder, an infectious-disease modeler at Harvard Medical School and Boston Children’s Hospital.
That said, a lot of people are still undoubtedly catching the coronavirus from people who aren’t feeling sick. Infection per infection, the risk of superspreading events might now be lower, but at the same time people have gotten chiller about socializing without masks and testing before gathering in groups—a behavioral change that’s bound to counteract at least some of the forward shift in symptoms. Presymptomatic spread might be less likely nowadays, but it’s nowhere near gone. Multiply a small amount of presymptomatic spread by a large number of cases, and that can still seed … another large number of cases.
There could be some newcomers to the pool of silent spreaders, too—those who are now transmitting the virus without ever developing symptoms at all. With people’s defenses higher than they were even a year and a half ago, infections that might have once been severe are now moderate or mild; ones that might have once been mild are now unnoticeable, says Seyed Moghadas, a computational epidemiologist at York University. At the same time, though, immunity has probably transformed some symptomless-yet-contagious infections into non-transmissible cases, or kept some people from getting infected at all. Milder cases are of course welcome, Fitzpatrick told me, but no one knows exactly what these changes add up to: Depending on the rate and degree of each of those shifts, totally asymptomatic transmission might now be more common, less common, or sort of a wash.
Better studies on transmission patterns would help cut through the muck; they’re just not really happening anymore. “To get this data, you need to have pretty good testing for surveillance purposes, and that basically has stopped,” says Yonatan Grad, an infectious-disease epidemiologist at Harvard’s School of Public Health.
Meanwhile, people are just straight-up testing less, and rarely reporting any of the results they get at home. For many months now, even some people who are testing have been seeing strings of negative results days into bona-fide cases of COVID—sometimes a week or more past when their symptoms start. That’s troubling on two counts: First, some legit COVID cases are probably getting missed, and keeping people from accessing test-dependent treatments such as Paxlovid. Second, the disparity muddles the start and end of isolation. Per CDC guidelines, people who don’t test positive until a few days into their illness should still count their first day of symptoms as Day 0 of isolation. But if symptoms might sometimes outpace contagiousness, “I think those positive tests should restart the isolation clock,” Popescu told me, or risk releasing people back into society too soon.
American testing guidelines, however, haven’t undergone a major overhaul in more than a year—right after Omicron blew across the nation, says Jessica Malaty Rivera, an infectious-disease epidemiologist at Boston Children’s Hospital. And even if the rules were to undergo a revamp, they wouldn’t necessarily guarantee more or better testing, which requires access and will. Testing programs have been winding down for many months; free diagnostics are once again growing scarce.
Through all of this, scientists and nonscientists alike are still wrestling with how to define silent infection in the first place. What counts as symptomless depends not just on biology, but behavior—and our vigilance. As worries over transmission continue to falter and fade, even mild infections may be mistaken for quiet ones, Grad told me, brushed off as allergies or stress. Biologically, the virus and the disease may not need to become that much more muted to spread with ease: Forgetting about silent spread may grease the wheels all on its own.