Exposure to common cold virus may protect from COVID-19: Study
Exposure to the rhinovirus, that causes the common cold infection can provide protection against infection by the SARS-CoV-2, the virus behind the COVID-19 pandemic, according to a study. The research, published on Tuesday in the Journal of Experimental Medicine, found that rhinovirus jump-starts the activity of interferon-stimulated genes. Here are more details.
- Triggering of early defenses can prevent or treat COVID-19 infection
- Interferon-stimulated genes can prove to be protective
- An artificially infected lab-grown human airway tissue was used
- Viral load at the time of exposure also matters
- Samples of patients diagnosed with initial infection were also studied
- Virus replicates exponentially before triggering a strong defense response
- Interferon treatment can possibly work better as a prevention
Triggering of early defenses can prevent or treat COVID-19 infection
"These genes trigger early-response molecules in the immune system which can stop reproduction of the SARS-CoV-2 virus, within airway tissues infected with the cold," the researchers said. "Triggering these defenses early in the course of COVID-19 infection holds promise to prevent or treat the infection," said senior study author, Ellen Foxman, Assistant Professor at the Yale School of Medicine in the US.
Interferon-stimulated genes can prove to be protective
Previous work showed that at the later stages of COVID-19, high interferon levels are associated with worse disease outcomes, and may fuel overactive immune responses. However, recent genetic studies show that interferon-stimulated genes can also be protective in cases of COVID-19 infection. The researchers wanted to study this defense system early in the course of COVID-19 infection.
An artificially infected lab-grown human airway tissue was used
The team infected lab-grown human airway tissue with the virus and found that for the first three days, viral load in the tissue doubled about every six hours. However, the researchers found that reproduction of SARS-CoV-2 virus was completely stopped in tissue that had been exposed to rhinovirus. If antiviral defenses were blocked, the SARS-CoV-2 could reproduce in airway tissue previously exposed to rhinovirus.
Viral load at the time of exposure also matters
The same defenses slowed down SARS-CoV-2 infection even without rhinovirus, but only if the infectious dose was low. "This suggests that the viral load at the time of exposure makes a difference in whether the body can effectively fight the infection," the researchers noted.
Samples of patients diagnosed with initial infection were also studied
Researchers also studied nasal swab samples from patients diagnosed with initial 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 defenses. The findings suggest the virus typically increased rapidly for the first few days of infection, before host defenses kicked in, doubling about every six hours as seen in the lab.
Virus replicates exponentially before triggering a strong defense response
In some patients the virus grew even faster, the researchers found. "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 defense response," Foxman said.
Interferon treatment can possibly work better as a prevention
Foxman explained that 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. "In theory, interferon treatment could be used as a preventive in people at high risk who have been in close contact with others diagnosed with COVID-19," the researchers said.
