(Natural News) Researchers from Yale University found that exposure to rhinovirus, the most common virus that causes the cold, can jump-start the immune system and protect people against the Wuhan coronavirus (COVID-19).
The presence of the virus that causes the common cold can begin the activity of interferon-stimulated genes. These are some of the early-response molecules in the immune system. If a person with the cold inhales SARS-CoV-2, the virus that causes COVID-19, there is a chance that it cannot replicate if it lands in the same airway tissues that are infected with the cold. (Related: If you’ve ever had a cold, your immune system may already know how to fight COVID-19.)
The new study, published on Tuesday, June 15 in the Journal of Experimental Medicine, examined rhinoviruses. These researchers had previously found that the immune system’s response to the common cold can protect people against the flu. They wanted to see if this kind of response could be replicated and offer similar protection against COVID-19.
They used human airway tissue grown in a lab for this experiment. The researchers infected the artificial tissue with the rhinovirus and then with the coronavirus. After the tissue was exposed to the rhinovirus, its immune system was automatically activated. The tissue with the rhinovirus was then infected with SARS-CoV-2. The virus was completely stopped from replicating.
The team compared the results by infecting a clean piece of lab-grown tissue with the coronavirus. They found that the viral load in this sample of tissue doubled every six hours.
They also found out that the body can slow down the spread of SARS-CoV-2 even without an initial rhinovirus infection if the infectious dose was very low. This suggests that the viral load at the time of exposure makes a difference in whether the body can fight off the coronavirus.
Triggering immune system responses early can prevent coronavirus infection
Ellen Foxman, senior author of the study, said there is a chance people can prevent a COVID-19 infection or treat it early by triggering these immune system responses. Foxman is also an assistant professor of laboratory medicine and immunobiology at Yale’s School of Medicine.
“But it all depends upon the timing,” said Foxman. “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.”
One way Foxman said people can trigger their immune systems is by treating early-stage COVID-19 patients with interferon, an immune system protein.
Foxman explained that interferon treatment holds promise, but it is very tricky. Interferon might only be effective in the days immediately after a person gets infected with COVID-19. During this time, the infection is still spreading and most people still do not have any symptoms.
She adds that, at least in theory, people at high risk of getting COVID-19 or who have been in close contact with people diagnosed with the virus could use interferon as a prophylactic.
In fact, trials studying interferon’s effectiveness in dealing with COVID-19 are already underway. Preliminary data from these studies shows there is a possible benefit to using interferon early in infection, but not when it is given during its later stages.
Foxman and the other researchers believe their study can help explain why at times of the year when colds are more common, rates of infections with other viruses like influenza tend to decrease. This interference between different respiratory viruses could mitigate the spread of other, deadlier viruses by creating an “upper limit” on the degree to which they could co-circulate.
“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,” said Foxman.