Rhinovirus Responsible for Common Cold Might Be Able to Boot COVID-19

Rhinoviruses, the common culprit behind the common cold, appear to kick the SARS-CoV-2 virus to the curb, theoretically providing some level of protection from COVID according to researchers from Scotland.

The cells in your nose, throat, and lungs are sanctuaries for viruses. When a virus enters it can either dominate the other cells or let other viruses share the abode.

Influenza is a great example of a virus hoarding sanctuaries not allowing other viruses to infect the same host. While adenoviruses tend to share the abode with other viruses.

Researchers speculate how COVID fits into the virus-virus relationship, with social distancing measures making it more difficult for scientists to get to the bottom of things.

But a recent study seems to crack the code on how common cold viruses can boot COVID out.

Rhinoviruses and COVID-19

A study published in the Journal of Infectious Diseases entitled, "Human rhinovirus infection blocks SARS-CoV-2 replication within the respiratory epithelium: implications for COVID-19 epidemiology" led by researchers from the MRC-University of Glasgow Centre for Virus Research shows that the human rhinovirus (HRV) blocks the replication of SARS-CoV-2 in respiratory tract cells.

Simply put, if you have HRV and SARS-CoV-2 virus in a petri dish of cultured human bronchial cells, COVID will struggle to take hold while the rhinovirus infection reigns supreme.

Professor Lawrence Young, a professor of Molecular Oncology at Warwick Medical School, not involved in the study comments that the effect observed was irrespective of whether viruses were used as simultaneous co-infection or staggered.

The inhibitory effect observed by scientists was likely due to HRV sparking an innate immune response in human bronchial cells.

(Photo: Photo by Andrea Piacquadio from Pexels)

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HRV and COVID Interaction

The study shows that the inhibitory effect was mostly due to HRV inducing a robust activation of the body's interferon-mediated innate immune response where the interferon response significantly reduced COVID infection, explains Young.

Scientists showed that if rhinovirus and SARS-CoV-2 were simultaneously released, only the HRV would be successful. On the other hand, if HRV had a 24-hour head start, then the COVID-19 causing virus would get booted by HRV.

Researchers utilized mathematical models to see whether HRV infections could outcompete COVID infection in a simulated population. As theorized, researchers found that new COVID infections decreases as the number of rhinoviruses increased suggesting that the common cold virus has the power to halt the spread of COVID in a population.

Dr. Julian Tang, an honorary associate professor in clinical virology at the University of Leicester, not involved with the study says that virologists have long known the viral interferences between HRV and seasonal influenza. The fact that HRV can also interfere with SARS-CoV-2 infections is intriguing and will need further scientific confirmation.

Young adds that the study suggests common infections could significantly impact the burden of COVID and influence its spread over autumn and winter months when seasonal colds are more frequent.

The relationship between HRV and COVID has only been tested in controlled laboratory tests and findings should be taken with a grain of salt.