It’s hard to envision the common cold, caused by rhinoviruses, as something of a superhero, but recent research from Yale University has found this bug to have an intriguing effect on the early success of the pathogen that causes COVID-19 in the body. Published in the Journal of Experimental Medicine, the research found that the common respiratory virus was able to halt the replication of SARS-CoV-2 as it triggered interferon-stimulated genes, which are some of the body’s first responders in an immune response. It’s possible, then, that interferon could play a pivotal role in the treatment of COVID-19, which has already claimed more lives in 2021 than the whole of 2020, but, as the researchers explain, timing is everything.
Senior author Dr Ellen Foxman, assistant professor of laboratory medicine and immunobiology at the Yale School of Medicine, wanted to look at the role of interferon-stimulated genes in the early stages of COVID-19 infection. Previous studies at Foxman’s lab had found that common cold viruses may protect against influenza, so they decided to once again employ rhinovirus, this time in the fight against the COVID-19 pathogen: SARS-CoV-2.
Foxman and team infected lab-grown human airway tissue with SARS-CoV-2 and measured what came next. The results revealed that for the first three days viral load in the tissue was roughly doubling every six hours. When they tried the same thing with tissue that had been exposed to rhinovirus, replication of SARS-CoV-2 was completely stopped. However, if tissue exposed to rhinovirus had its antiviral defenses blocked, SARS-CoV-2 was once again able to replicate. So, could it be that simply catching a cold can be the difference between severe and mild COVID-19 symptoms?
"Our study implies that being infected with the common cold could protect you from COVID-19," Foxman told IFLScience. "Our results show that the common cold is very good at activating the general antiviral defenses (also called the “antiviral interferon response”), that broadly protect against many viral infections, including SARS-CoV-2.
"We know that these defenses, interferon responses, are particularly important for fighting COVID-19. The virus does everything it can to block these defenses once it infects you. However, we found that if these defenses are pre-activated by a different virus, this is a work-around that allows a strong defense against SARS-CoV-2 right from the start of infection."
Those same antiviral defenses are known to slow the replication of SARS-CoV-2 even when rhinovirus has played no part, but their efficacy hinges on a person being exposed to a small viral load at the time of infection. This is why policies surrounding social distancing remain important, as sitting opposite a friend outside or indoors can be the clincher between a fleeting puff or fat drop of SARS-CoV-2 entering your system.
The study also looked at nasal swab samples from infected humans in the early days of COVID-19. Their analyses revealed that, like the lab tissue, SARS-CoV-2 was rapidly replicating in the early days of infection, only after which did the body’s defenses start to kick in. This delay between infection and the body's response is what Foxman refers to as a "viral sweet spot" in the progression of COVID-19 as it replicates, a time at which interferon could potentially play a crucial role in stopping disease progression. However, the complication arises in getting the treatment to the patient in such a small – and usually asymptomatic – window of disease.
The next step is to establish if interferon could be used safely and effectively as a prophylactic treatment for those who are at high risk of hospitalization from COVID-19, as well as those having frequent contact with others diagnosed with the disease. Trials investigating this are reportedly already underway and have so far shown that it may glean a benefit in the early stages of infection, but not when given late. Foxman also hopes to gain a better understanding of how the presence and absence of viruses alters the severity of subsequent infections.
"We would like to understand how the interactions among viruses, like the ones that we describe in this study, affect susceptibility to respiratory viruses in general," Foxman told IFLScience. "There are about 15 common respiratory viruses that cause colds and flu, and there is still a lot we don’t understand about how they spread and cause disease.
"Over the past several years, there is more and more evidence that interactions among respiratory viruses are important in determining who is susceptible at a given time. These interactions may also be shaping how cold and flu viruses spread throughout the world each year. Understanding how one infection impacts susceptibility to another could lead to new therapies for respiratory viruses and new ways to protect against future pandemics."