Exposure to this common seasonal virus may protect you from COVID-19.
New study found that cells exposed to rhinovirus, the most common cause of the common cold, gain protection from the SARS-CoV-2 virus.
The study, led by American researchers from Yale University, found that the common respiratory rhinovirus activates a group of genes called ‘interferon-stimulated genes’ (IS genes). These genes function as first-response molecules within the immune system, preventing the replication of the SARS-CoV-2 virus in human airway tissue.
The study, led by Prof Ellen Foxman, from the Yale School of Medicine, in New Haven, Connecticut, USA, and published earlier this week, may help design new therapies against SARS-CoV-2 infection.
“Triggering these defences early in the course of COVID-19 infection holds promise to prevent or treat the infection,” Prof Foxman said in a press release. The main idea would be treating patients with interferons, a type of protein involved with the immune system, Prof Foxman explains.
About the findings
Previous research has shown a significant correlation between interferon levels and COVID-19 disease severity. Previous research from Prof Foxman’s team has showed that common cold viruses can have a protective affect against influenza. Now, her team wanted to know if the same defence system could work against the COVID-19 virus.
In this new study, researchers infected lab-grown human airway tissue with SARS-CoV-2, and found, as expected, rapid growth of the virus, with the viral load doubling every six hours. However, when the tissue was exposed to rhinovirus, replication of the COVID-19 virus stopped completely. But if the antiviral defences were experimentally blocked, the SARS-CoV-2 could replicate again, even if the tissue had been previously exposed to rhinovirus.
The study also found that this defence mechanism, involving IS genes, could slow down SARS-CoV-2 infection, even without rhinovirus infection, but only at low doses of viral infection. This suggests that the initial viral load influenced whether the body can effectively fight SARS-CoV-2 infection.
Researchers also found evidence that SARS-CoV-2 goes through a rapid growth phase during the first days of infection, before the body’s defence activates.
“There appears to be a viral sweet spot at the beginning of COVID-19, during which the virus replicates exponentially before it triggers a strong defence response,” Prof Foxman said. “Interferon treatment holds promise but it could be tricky, because it would be mostly effective in the days immediately after infection, when many people exhibit no symptoms,” she added.
Still, interferon treatment has the potential to be used prophylactically in people at high risk who have been in close contact with infected people.
“These findings may help explain why at times of year when colds are common, rates of infections with other viruses such as influenza tend to be lower,” Prof. Foxman said. “There are hidden interactions between viruses that we don’t quite understand, and these findings are a piece of the puzzle we are just now looking at,” she added.