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-stimulation genes, early response molecules in the immune system which can halt the replication of the SARS-CoV-2 virus within airway tissue infected with the cold.
Triggering these defences early in the course of COVID-19 infection holds promise to prevent or treat the infection, said Ellen Foxman, Assistant Professor of Laboratory Medicine 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 that is also available as a drug. “But it depends upon the timing”, Foxman said.
Foxman lab showed that common cold viruses may protect against influenza, so 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 in 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 defences were blocked, the SARS-CoV-2 could replicate in airway tissue previously exposed to rhinovirus.
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The same defences 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.
The researchers also studied nasal swab samples from patients diagnosed close to the start of infection, they found evidence of rapid growth of SARS-CoV-2 in the first few days of infection, followed by activation of the body’s defences, According to their findings, the virus typically increased rapidly for the first few days of infection before host defences kicked in, doubling about every six hours as seen in the lab, in some patients the virus grow even faster.
“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”, Foxman said.
Interferon treatment holds promise but it could be tricky, she said, because it would be most effective in the days immediately after infection when many people exhibit no symptoms.
In theory, interferon treatment could be used prophylactically in people at high risk who have been in close contact with others diagnosed with COVID-19. Trials of interferon in COVID-19 are underway, and so far show possible benefits early in infection but not when given later.
These findings may help explain why at the times of the year when colds are common, rates of infection with other viruses such as influenza tend to be lower, Foxman said. There are concerns that as social distancing measures ease, common cold and flu virus- which have been dormant over the past year will come back in greater force. Interference among respiratory viruses could be a mitigating factor, creating an “upper limit” on the degree to which respiratory viruses co-circulate, She said.
“There are hidden interactions between the virus that we don’t quite understand and these findings are a piece of the puzzle we are just now looking at,” Foxman added.
