- In a lab study, researchers discovered that a virus that causes the common cold can induce an innate immune response to SARS-CoV-2, the virus that causes COVID-19.
- In principle, infections with the common cold virus could stop SARS-CoV-2 from spreading through a population and make infections less serious.
- Further research may lead to control strategies or therapies that take advantage of such viral interactions.
Scientists have been searching for a cure for the common cold for decades, with little success.
Recent research suggests, however, that this bothersome — although normally mild — infection may be a hidden ally in the battle against pandemic viruses like influenza and SARS-CoV-2.
Human rhinoviruses (HRVs) are the most common respiratory viruses in humans, accounting for more than half of all common colds.
HRVs may have delayed the spread of the influenza A virus subtype H1N1 across Europe during the 2009 flu pandemic, according to previous reports.
HRVs are thought to have achieved this by inducing human cells to produce interferon, a protein that is part of the body’s natural immune response to viral infection.
SARS-CoV-2 has been shown to be sensitive to the effects of interferon.
This observation prompted researchers at the MRC-University of Glasgow Centre for Virus Research in the United Kingdom to wonder if HRVs could help stop SARS-CoV-2 from spreading and limiting the severity of infections.
Human respiratory cells
To find out, the researchers contaminated human respiratory cell cultures in the lab with SARS-CoV-2, HRV, or both viruses at the same time.
The cultures closely resembled the epithelium, the outer layer of cells that forms the lungs’ airways.
SARS-CoV-2 multiplied steadily in cells infected solely with this virus, according to the researchers. The number of SARS-CoV-2 virus particles in cells infected with HRV, on the other hand, rapidly decreased until they were undetectable just 48 hours after infection.
In additional experiments, the researchers discovered that HRV inhibited SARS-CoV-2 replication regardless of which virus infected the cells first.
SARS-CoV-2, on the other hand, had no effect on HRV development.
The researchers repeated their experiments in the presence of a molecule that inhibits the effects of interferon to see whether HRV was inhibiting SARS-CoV-2 by activating the cells’ innate immune response.
SARS-CoV-2 replication was restored in cells infected with HRV after the molecule was introduced.
“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.
Prof. Murcia continues, “This suggests that the immune response elicited by moderate, common cold virus infections could provide some form of temporary defense against SARS-CoV-2, potentially blocking transmission and reducing the severity of COVID-19.”
The researchers used a mathematical model to predict how different numbers of HRV infections of differing lengths will influence SARS-CoV-2 spread in a population.
The findings revealed that the number of new SARS-CoV-2 infections is inversely proportional to the number of HRV infections in a population.
The model predicts that if the common cold virus spreads widely and persistently enough, it would temporarily stop SARS-CoV-2 from spreading.
“The next step will be to investigate what happens at the molecular level during these virus-virus interactions in order to better understand their effects on disease transmission,” Prof. Murcia says.
“We can then use this knowledge to our advantage, hopefully developing strategies and control measures for COVID-19 infections,” he adds.
The findings were published in the Journal of Infectious Diseases.
Mild HRV infections, the researchers speculate in their paper, may be beneficial to both the virus and its human hosts.
The immune system may have evolved to allow HRV to replicate and spread to new hosts, they write. In exchange, the virus prevents more serious and potentially fatal viral infections.
Other scientists at the Science Media Centre in London, United Kingdom, praised the study but pointed out several possible drawbacks.
The study’s major limitation, according to Gary McLean, a professor of molecular immunology at London Metropolitan University in the United Kingdom, was that it only looked at one of the 160 or more potential rhinovirus strains.
He said there was no guarantee that each strain would affect SARS-CoV-2 infections in the same way.
He added that translating results from a lab experiment to real life is “very tricky,” saying:
“Although a common cold virus, such as rhinovirus, is likely to elicit a powerful innate immune response capable of blocking SARS-CoV-2 infections, both infections must occur at the same time.”
Furthermore, he noted that over the past year, intensive infection prevention efforts have reduced the prevalence of the common cold, decreasing the capacity for HRV-triggered innate immunity to fight the spread of SARS-CoV-2.