fb-pixel Skip to main content

A potential saving grace in the next cold and flu season

There’s increasing evidence for the idea that getting one virus offers some protection against another.

A cell infected with the virus that causes COVID-19.NATIONAL INSTITUTES OF HEALTH/NYT

As mask mandates end and workplaces and schools reopen, viruses long held in check by precautions against COVID-19 are making comebacks. And they’ll be infecting a population in which relatively few people have picked up any immunity to them since the pandemic began. Are we headed for a year of nonstop sniffles and coughs and even worse?

Not necessarily. Researchers studying how COVID-19 and the common cold interact with the body’s immune system suggest that as we return to a semblance of normalcy, an underappreciated phenomenon called viral interference may help put some limits on the next cold and flu season.


Immunologists have known for some time that one virus can get in the way of another. Last year, Ellen Foxman, an immunologist at Yale Medical School, and colleagues found that rhinoviruses, which cause the common cold, can protect against a later infection by a flu virus. Using lab-grown models of human airway tissue, they discovered that part of our innate immune system, the interferon response, stays activated for days after a rhinovirus switches it on.

As a result, influenza A virus couldn’t grow in the airway; its numbers stayed low rather than rising exponentially. This helped explain a peculiar observation made by epidemiologists a decade ago: The fall 2009 cold season in France seems to have delayed the start of the swine flu pandemic there.

The immune activation caused by rhinoviruses also can fight off SARS-CoV-2, the coronavirus that causes COVID-19, Pablo Murcia at the University of Glasgow and colleagues reported in January.

This month, in a new study in the Journal of Experimental Medicine, Foxman and colleagues confirmed those results. Using model airways, they saw that the cold virus kept SARS-CoV-2 from growing. To understand how, they looked at the interferon response caused by SARS-CoV-2 on its own, without rhinovirus. They drew on samples and test results from patients at Yale-New Haven Hospital who were at different stages and severities of COVID-19 infection.


They found that the immune system’s interferon response is generally low at first and increases days after the infection begins. That gives the virus a window of opportunity to replicate freely in the upper airway. A rhinovirus infection would deprive SARS-CoV-2 of this window, says Foxman, stalling it before it even got started.

Might other viruses, like the flu and respiratory syncytial virus, which is currently on the rise in the South, interact in a similar way and provide protection against back-to-back illnesses?

Definitively answering that question will require careful study of the relationships between viruses, Murcia cautions. But in their study, Foxman and colleagues hypothesize that the answer might be yes: Even if we face a rise in cases of viruses generally, their spread may be slowed somewhat by the fact that the first of these infections will activate people’s interferon responses.

“Once the transmission cycle begins, there may be a silver lining, that there is an upper limit,” she speculates. “Once we all start getting colds, we’ll now have reawakened our innate immune system in the upper respiratory tract, and that may mitigate the extent to which things can simultaneously circulate or just infect people one after another.”

However, it’s not clear if children have the same innate immune response as adults, she notes. And although viral interference could hold down the number of viral infections during reopening, the effect isn’t likely to be as dramatic as the effects of social distancing and other COVID-19 precautions.


“It’s going to be a very important year to observe and see what happens,” Foxman says.

Veronique Greenwood is a writer whose work has appeared in such publications as The New York Times, The Atlantic, and National Geographic.