NEW HAVEN - Catching a cold may protect against the coronavirus, according to research at the Yale School of Medicine. A new study has found that rhinovirus, source of the common cold, activates interferon-stimulated genes, which are early responders in the immune system that can stop the coronavirus, SARS-CoV-2, from replicating inside the rhinovirus-infected cells. Dr. Ellen Foxman, assistant professor of laboratory medicine and immunobiology at the Yale School of Medicine and senior author of the study, said treating patients with interferons, an immune system protein, can activate the genes and prevent or treat COVID-19. "But it all depends upon the timing," Foxman said. High interferon levels have been seen in patients with serious cases of COVID, and may overstimulate the immune system, but Foxman wanted her lab to look at what happens early in a coronavirus infection because earlier studies showed that cold viruses could protect against influenza. The study was conducted on lab-grown human airway tissue infected with the coronavirus, which doubled every six hours. But it was completely stopped in tissue that had been exposed to rhinovirus, the release stated. "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 said in the release. The immune defenses also worked if the initial coronavirus exposure was low, suggesting that how much virus the body is exposed to may make a difference in the seriousness of COVID. The catch is that many people with coronavirus infection do not have symptoms early on, when interferon would do the most good. The results were published June 15 in the journal Journal of Experimental Medicine. In another study, Dr. Hyung Chun, co-director of the Yale Cardiovascular Research Center, found that three proteins found in the blood of post-COVID patients appeared to predict who may have long-term symptoms of the disease. The proteins found in the blood, known as biomarkers, are lipocalin 2, matrix metalloproteinase 7, and hepatocyte growth factor, which are strongly associated with impaired lung function, according to a press release. "We wanted to get a better understanding of what is driving the disease process in patients who had persistent symptoms after their COVID-19 infection," said Chun. The study, published June 10 in the journal JCI Insight, follow an earlier study in which Chun and his colleagues discovered that lipocalin 2 and hepatocyte growth factors predicted which patients were more likely to suffer severe COVID and require intensive care, according to the release. Chun believes the biomarkers may not only be associated with more severe symptoms, but also may be a part of the the disease process itself, the release said.