Viruses which cause the common cold may protect against COVID-19, new research suggests.
Rhinoviruses, source of the common cold, activate interferon-stimulated genes – early responders in the immune system – which can stop COVID-19 from replicating in rhinovirus-infected airway tissues.
But these defences must be triggered early in COVID-19 infection, explains Dr Ellen Foxman, assistant professor at the Yale School of Medicine, USA.
In the laboratory, her team infected human airway tissue with SARS-CoV-2 and found that replication of the virus was completely halted in tissue which had been exposed to rhinovirus.
Further tests showed that the same defence pathway, activated by interferon given as a drug, slowed down COVID-19 infection. But this was only effective when the viral load was low.
In patients, COVID-19 viral load typically increases rapidly for the first few days of infection, doubling about every six hours. Once viral load is high, raised interferon levels are linked to worse disease.
Dr Foxman says: "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.
"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."
Trials are underway, and the team suggest that, in theory, interferons could be given prophylactically to high-risk people who have been exposed to others diagnosed with COVID-19.
Details were published yesterday in the <i>Journal of Experimental Medicine</i>.
Cheemarla, N. R. et al. Dynamic innate immune response determines susceptibility to SARS-CoV-2 infection and early replication kinetics. Journal of Experimental Medicine 15 June 2021; doi: 10.1084/jem.20210583
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