NEW HAVEN, Conn. — Cold and flu season is right around the corner, but that may be a good thing when it comes to combating COVID-19. A new study finds the common cold can actually help protect people from serious coronavirus infections.
Between the runny nose, sneezing, and coughing, there aren’t many positive aspects of catching a cold. One upside however, is that dealing with a cold virus generally prevents people from developing worse illnesses, like the flu.
Now, researchers at Yale University say exposure to the rhinovirus, one of the most frequent causes of the common cold, can trigger the proper immune responses patients need to defend against COVID-19 before an infection spreads. Their study finds this cold virus kickstarts the body’s interferon-stimulated genes. These are “early-response” molecules which help the immune system stop viruses from replicating. In the case of SARS-CoV-2, the virus causing COVID-19, interferons prevent the illness from multiplying in a patient’s airway tissue — which are already dealing with a cold.
Ellen Foxman from the Yale School of Medicine says triggering an early response to COVID looks like a promising way of dealing with the pandemic moving forward. One way scientists can do this is by treating coronavirus patients with interferons, an immune system protein, early on during their illness. Unfortunately, all of this depends on catching the virus at the right time.
“It all depends upon the timing,” the assistant professor of laboratory medicine and immunobiology says in a university release.
COVID has nowhere to go when you have a cold
Study authors note that previous studies on COVID-19 concluded that high interferon levels have a link to more serious cases of the illness. These reports added that more interferons could even trigger an overactive immune response — the so-called “cytokine storm.”
However, new genetic studies are now finding that interferon-stimulated genes can protect patients from coronavirus. Foxman’s team had previously shown that the common cold can protect people from the flu.
In their new report, researchers infected lab-grown human airway tissue with SARS-CoV-2. During the first three days, they discovered viral loads in the tissue doubled every six hours. In tissue exposed to rhinovirus however, the COVID-19 virus completed stopped replicating.
On the other hand, if the tissue’s antiviral defenses were blocked, the study finds SARS-CoV-2 could still replicate and spread through the rhinovirus-infected airway cells. Researchers also discovered that human immune defenses could slow down a COVID infection even without the common cold’s help, but this is only possible if the viral load is very low.
The team says this could mean the amount of coronavirus someone is initially exposed to is extremely important in determining how well they’ll be able to fight the infection.
Finding the COVID-19 ‘sweet spot’
The Yale team also examined nasal swabs from patients at the very beginning of their coronavirus infections. They discovered there is rapid virus growth within the first few days before the body’s defenses react.
“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 defense response,” Foxman explains.
With interferon treatments, the tricky part for researchers will be finding just the right time to treat patients. During the first few days of a coronavirus infection, a patient typically shows no symptoms of the illness, making it hard to know who’s really sick.
Study authors suggest people could receive interferon treatments as a preventative measure. Specifically, people at high risk for infection or who just came into contact with a COVID-positive person could take these treatments ahead of time.
Foxman says these findings also explain why cases of other viruses drop during times of the year when colds are more common.
“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,” Foxman concludes.
The results appear in the June 15 issue of the Journal of Experimental Medicine.