Why Hasn't This Research Been Converted Into A Prophylactic Nasal Spray?

yale |  Exposure to the rhinovirus, the most frequent cause of the common cold, can protect against infection by the virus which causes COVID-19, Yale researchers have found.

In a new study, the researchers found that the common respiratory virus jump-starts the activity of interferon-stimulated genes, early-response molecules in the immune system which can halt replication of the SARS-CoV-2 virus within airway tissues infected with the cold. 

Triggering these defenses early in the course of COVID-19 infection holds promise to prevent or treat the infection, said Ellen Foxman, assistant professor of laboratory medicine and immunobiology at the Yale School of Medicine and senior author of the study. One way to do this is by treating patients with interferons, an immune system protein which is also available as a drug.

“But it all depends upon the timing,” Foxman said.

The results were published June 15 in the Journal of Experimental Medicine.

Previous work showed that at the later stages of COVID-19, high interferon levels correlate with worse disease and may fuel overactive immune responses. But recent genetic studies show that interferon-stimulated genes can also be protective in cases of COVID-19 infection.

Foxman’s lab wanted to study this defense system early in the course of COVID-19 infection.

Since earlier studies by Foxman’s lab showed that common cold viruses may protect against influenza, they decided to study whether rhinoviruses would have the same beneficial impact against the COVID-19 virus. For the study, her team infected lab-grown human airway tissue with SARS-CoV-2 and found that for the first three days, viral load in the tissue doubled about every six hours. However, replication of the COVID-19 virus was completely stopped in tissue which had been exposed to rhinovirus. If antiviral defenses were blocked, the SARS-CoV-2 could replicate in airway tissue previously exposed to rhinovirus.

The same defenses slowed down SARS-CoV-2 infection even without rhinovirus, but only if the infectious dose was low, suggesting that the viral load at the time of exposure makes a difference in whether the body can effectively fight the infection.