File under: Nature is Amazing
In a new Yale-led study, researchers found that in patients with the COVID-19 infection only, antiviral defenses are low and SARS-CoV-2 viral load is high, as represented in the circle on the left. When patients also have the common cold early in the COVID-19 infection, antiviral defenses are high and SARS-CoV-2 viral load is low, as shown on the right.
Exposure to the rhinovirus, the most frequent cause of the common cold, can protect against infection by the virus which causes COVID-19, Yale researchers have found.
In a new study, the researchers found that the common respiratory virus jump-starts the activity of interferon-stimulated genes, early-response molecules in the immune system which can halt replication of the SARS-CoV-2 virus within airway tissues infected with the cold.
These findings may help explain why at times of year when colds are common, rates of infections with other viruses such as influenza tend to be lower, Foxman said. There are concerns that as social distancing measures ease, common cold and flu viruses — which have been dormant over the past year — will come back in greater force. Interference among respiratory viruses could be a mitigating factor, creating an “upper limit” on the degree to which respiratory viruses co-circulate, she said.
“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 said.
In sum, our results demonstrate an important role for IFN-mediated defenses in curtailing SARS-CoV-2 replication at the start of infection, including heterologous innate immune responses induced by prior RV infection. These results, and our findings in longitudinal patient samples, support the concept that airway innate immunity is dynamic, with innate immune defense rapidly changing in response to current and recent viral infections. Our findings also demonstrate that ISG-mediated defenses can profoundly curtail SARS-CoV-2 replication under certain conditions and compel further studies of the role of heterologous innate immunity in protecting against SARS-CoV-2 and other respiratory viruses.
