Your respiratory tract is as much an ecosystem as the rainforest or the savannah, virologists believe, lush with viruses and other pathogens that compete for resources and space. Sometimes, one virus gets caught in the immune system’s attack against another one. Such “viral interference,” where an infection protects against further infections, has not been widely studied.
But now, researchers at the University of Glasgow in Scotland report that the presence of a rhinovirus, which causes the common cold, keeps SARS-CoV-2 — the virus that causes COVID-19 — from replicating in human cells. It’s an intriguing finding suggesting that interference may reduce COVID-19 infection numbers and that understanding how it works could potentially lead to preventive therapies against viruses of all kinds.
Some years ago, Pablo Murcia, one of the new paper’s authors and a professor at the University of Glasgow, and his colleagues noticed that rhinoviruses and the flu tended to avoid each other. Patients with both infections were fewer than you’d expect, prompting the researchers to think that the viruses interfered with each other. Epidemiologists had a similar hunch after the 2009 pandemic flu failed to infect many people in France until after the fall cold season blew through.
In 2020, Ellen Foxman, an immunologist at Yale Medical School, and her colleagues found that human airway cells infected by a rhinovirus resisted infection by the flu some days later. They traced the effect to immune messengers called interferons, provoked in response to the cold virus and capable of keeping the flu virus from growing.
Could rhinoviruses have a similar effect on SARS-CoV-2? The new coronavirus is quite different from the flu. But the immune system uses the interferon response against many viruses, including, researchers found last year, SARS-CoV-2. So Murcia and colleagues infected cells with SARS-CoV-2 and rhinovirus at the same time and kept track of the coronavirus’s replication. They found that it could not replicate well in the presence of the rhinovirus. Indeed, it flopped, with its numbers undetectable by 48 hours after infection.
In a similar set of studies, currently available as a preprint, Foxman’s group found that for as long as six days after a rhinovirus infection, SARS-CoV-2 could not mount its usual takeover of airway cells.
These findings, Murcia says, imply that when cold viruses are circulating widely, they may be one of the forces protecting people from SARS-CoV-2, leading to lower case counts than one might expect.
They may protect against other viruses as well, more significantly that we realize, Foxman says: “Depending on how widely these viruses spread, these common colds could actually be a mitigating factor in reducing the spread of more dangerous viruses, as also suggested by our previous work on colds and flu.”
While vaccinations are far more certain ways to avoid both COVID and the flu, the researchers suggest that understanding how the interferon response has this effect could someday inspire treatments and preventive strategies.
From an evolutionary perspective, it’s possible that for humans and for rhinoviruses, this is a mutually beneficial arrangement. The rhinovirus gets a chance to dominate its environment, making free use of the resources in the ecosystem of your throat. And humans get a chance to avoid potentially life-threatening infections from other viruses — at least for a few days.
Veronique Greenwood is a writer whose work has appeared in The New York Times, The Atlantic, and National Geographic, among other publications.