New York: Researchers have identified specific proteins within our lungs that can protect us from SARS-CoV-2 infections, potentially opening the door to new antiviral therapies.
In the study, published in the journal Nature Genetics, researchers used CRISPR technology to test the impact of every human gene on SARS-CoV-2 infections in human lung cells.
Their findings revealed new pathways that the virus relies on to infect the cells, as well as the antiviral pathways that help protect against viral infection.
Notably, the team from the University of California-Berkeley showed that mucins — the main component of mucus found in the lungs — seem to help block the SARS-CoV-2 virus from entering our cells.
“Our data suggest that mucins play a key role in restricting SARS-CoV-2 infection by acting as a barrier to viruses that are attempting to access our lung epithelial cells, said Scott Biering, postdoctoral researcher at UC Berkeley’s School of Public Health.
“Further, our data suggest that mucin expression levels in an individual’s lungs may impact Covid progression,” Biering added.
Researchers discovered that MUC1 and MUC4, types of mucins found in lung cell membranes, defend lung cells from infection.
This finding is important because previous studies had suggested that an accumulation of mucus could be the reason why some people became seriously ill due to Covid infection, since the mucus can make it difficult for people to breathe and proposed using drugs to deplete mucus.
However, the new study suggests that such a strategy could interfere with mucins that provide a valuable defence mechanism against SARS-CoV-2 infection.
Further, the team discovered that other mucins — MUC5AC and MUC5B — which are secreted into the mucus lining of the lungs, either do nothing to stop SARS-CoV-2 infection or can even promote viral infection.
According to Biering, both the type and amount of mucus that each person produces may result in different outcomes for SARS-CoV-2 infection — and lead to different treatment strategies.
“Somebody who produces a lot of the right type of mucus could be very protected. But somebody who produces a lot of the wrong type of mucus might have more risk of infection,” said Biering. “And somebody who produces very little of the right type also could be at more risk.”
The team also studied how mucins would interact with other respiratory viruses, including influenza A virus, human parainfluenza virus, common cold coronaviruses and respiratory syncytial virus. As with SARS-CoV-2, the results were unpredictable, they found.
