The COVID-19 study found that exposure to a virus that causes the common cold can confer protection against SARS-CoV-2 infection.
A study published Tuesday in the Journal of Experimental Medicine found that rhinovirus, a common respiratory virus, triggers interferon-stimulated gene activity. These genes trigger early response molecules in the immune system that can stop replication of the SARS-CoV-2 virus, which causes COVID-19, in cold-infected respiratory tissues, the researchers say.
According to the study’s lead author, Ellen Foxman, assistant professor at Yale School of Medicine (USA), activation of these defense mechanisms in the early stages of COVID-19 infection holds promise for preventing or treating the infection.
One way to do this is to treat patients with interferons, an immune system protein that is also available in drug form, Foxman said. “But it all depends on the timing,” he said.
Previous work has shown that, in late-stage COVID-19 disease, elevated interferon levels are associated with worse disease progression and may promote overactive immune responses. However, recent genetic studies suggest that interferon-stimulated genes may also be protective in COVID-19 infection.
The researchers wanted to study this defense system in the early stages of COVID-19 infection. They decided to investigate whether rhinoviruses could have a beneficial effect against SARS-CoV-2.
However, the researchers found that COVID-19 replication was completely stopped in tissue exposed to rhinovirus. When antiviral protection was blocked, SARS-CoV-2 was able to replicate in respiratory tissue previously exposed to rhinovirus.
The same protectants delayed SARS-CoV-2 infection by SARS pneumonia even in the absence of rhinovirus, but only when the infectious dose was low. This suggests that viral load at the time of infection is a key determinant of whether the organism can effectively fight infection, the researchers said.
The research team also examined nasal swab samples from patients diagnosed near the onset of infection. They showed rapid growth of SARS-CoV-2 in the first days after infection, followed by activation of the body’s defenses.
According to their findings, the virus tends to replicate rapidly in the first days of infection, before the host’s defenses kick in, doubling in size approximately every six hours, as seen in the laboratory. The virus grew even faster in some patients, the researchers found.
“There appears to be a favorable viral point early in COVID-19 disease where the virus replicates exponentially before eliciting a strong protective response,” Foxman said. He explained that treatment with interferon is promising, but can be difficult because it is most effective in the first few days after infection, when many people have no symptoms.
In theory, interferon treatment could be used as a preventive measure in high-risk individuals who have had close contact with others diagnosed with COVID-19, they said. COVID-19 interferon is currently being tested and so far has shown potential benefit in the early stages of infection, but not when administered later.
These findings may explain why infection rates for other viruses, such as influenza, tend to be lower during times of the year when colds are prevalent, Foxman said.