A common cold virus may help fight COVID-19

A common cold virus may help fight COVID-19


Written by James Kingsland on March 29, 2021 — Fact checked by Hilary Guite, FFPH, MRCGP
Share on PinterestA recent study asks whether a common virus might help fight COVID-19. Photo edited by Stephen Kelly; Photography courtesy of Thomas Splettstoesser/Wikimedia

  • A lab-based study has found that a virus that causes the common cold can trigger an innate immune response against SARS-CoV-2, the virus responsible for COVID-19.
  • In theory, infections with the common cold virus could inhibit the transmission of SARS-CoV-2 among members of a population and reduce the severity of infections.
  • Further research could lead to control strategies or treatments that exploit such interactions between viruses.

For decades, scientists have been hunting for a cure for the common cold, with little success.

However, recent research hints that this bothersome — though usually mild — infection may be a hidden ally in the fight against pandemic viruses such as influenza and SARS-CoV-2.

Human rhinoviruses (HRVs), which cause more than half of all common colds, are the most widespread respiratory viruses in humans.

Stay informed with live updates on the current COVID-19 outbreak and visit our coronavirus hub for more advice on prevention and treatment.

Previous research suggests that HRVs may have inhibited the spread of the influenza A virus subtype H1N1 across Europe during the 2009 flu pandemic.

Experts believe that the HRVs did this by inducing human cells to produce interferon, which is part of the body’s innate immune defenses against viral infection.

Research has shown that SARS-CoV-2 is susceptible to the effects of interferon.

This finding led scientists at the MRC-University of Glasgow Centre for Virus Research in the United Kingdom to speculate whether HRVs could help combat the spread of SARS-CoV-2 and limit the severity of infections.

Human respiratory cells

To find out, the researchers infected cultures of human respiratory cells in the lab with either SARS-CoV-2, an HRV, or both viruses at the same time.

The cultures closely mimicked the outer layer of cells, called the epithelium, that lines the airways of the lungs.

SARS-CoV-2 steadily multiplied in the cells that the team had infected with this virus alone. However, in cells also infected with HRV, the number of SARS-CoV-2 virus particles declined rapidly until they were undetectable just 48 hours after the initial infection.

In further experiments, the scientists found that HRV suppressed the replication of SARS-CoV-2, regardless of which virus infected the cells first.

Conversely, SARS-CoV-2 had no effect on the growth of HRV.

To test their hunch that HRV was inhibiting SARS-CoV-2 by triggering the cells’ innate immune response, the researchers repeated their experiments in the presence of a molecule that blocks the effects of interferon.

Sure enough, the molecule restored the ability of SARS-CoV-2 to replicate in cells infected with HRV.

“Our research shows that human rhinovirus triggers an innate immune response in human respiratory epithelial cells, which blocks the replication of the COVID-19 virus, SARS-CoV-2,” says senior author Prof. Pablo Murcia.

“This means that the immune response caused by mild, common cold virus infections could provide some level of transient protection against SARS-CoV-2, potentially blocking transmission of SARS-CoV-2 and reducing the severity of COVID-19,” Prof. Murcia adds.

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