Advanced technology (CRISPR) shows that mucus is the body's first line of defense against viruses

This article on CRISPR is part of an extended series on regenerative medicine. For more stories on this topic, williamhaseltine.com Search for regenerative medicine. My definition of regenerative medicine is any medical modality that restores us to a state of normal health following injury from disease, injury from trauma, disability from birth, or wear and tear over time. Modalities include chemicals used as drugs, genes, proteins, cells, gene editing, prosthetics, and mind-machine interfaces.

One of the key mysteries of SARS-CoV-2 is why some people seem to be infected more severely than others. Vaccines have provided much-needed protection against viruses, but there is still a need to develop better drugs to treat infected people.

A major way to develop drugs to combat viral infections is to determine what the virus needs to replicate in the body. To date, most research has focused solely on SARS-CoV-2 and its unique attack methods. However, infection requires cooperation between the virus and the cells of the human body. In fact, viruses rely on many cellular structures within the host cell to replicate.

So how can we decipher SARS-CoV-2 and its interaction with our own bodies? It is to conduct a systematic study of all genes in a cell. By inhibiting most genes while leaving some genes active, scientists can pinpoint exactly which genes and cell structures influence SARS-CoV-2 infection.

Fortunately, using a new gene-editing tool called CRISPR, researchers at the University of California, Berkeley were able to do just that. After conducting a study of genes found in lung cells, Biering et al. have discovered a naturally occurring protein in the body that may have the ability to inhibit SARS-CoV-2 infection. This study is the first to examine how SARS-CoV-2 interacts with human lung cells and represents an important advance in SARS-CoV-2 research.

How does CRISPR work? CRISPR technology is the latest advance in gene editing. The technology consists of her two components, Cas9, an enzyme that cuts DNA, and a short RNA segment that guides Cas9. When the guide RNA finds a complementary sequence in DNA, it binds to the target gene and acts as a signal to the Cas9 enzyme. Once Cas9 finds and binds to the guide RNA, the enzyme can cleave the entire DNA sequence at that specific position. This allows scientists to completely knock out genes or insert new genes to edit the genome.

beer ring etc. We used CRISPR technology to study the genes present in human lung epithelial cells. Epithelial cells line the walls of the lungs and are responsible for producing mucus and initiating several immune responses. Lung epithelial cells also express receptors such as ACE2, which are known to affect SARS-CoV-2 infection, making the cells a valuable model for SARS-CoV-2 infection.

After studying the effects of each gene found in lung epithelial cells, Biering et al. We have found several genes that appear to influence SARS-CoV-2 infection. These included not only known genes, such as those responsible for the ACE2 receptor, but also some new players. It was a group responsible for the production of

Mucins are the most abundant proteins found in mucus and can either be secreted to form gels over the surface of the lung or reside within epithelial cell membranes. We found that only the mucins in the cell membrane appear to directly affect the severity of SARS-CoV-2.

To determine whether membrane-bound mucins can exert antiviral effects against SARS-CoV-2 infection, Biering et al. then overexpressed the mucins. Surprisingly, membrane-bound mucin successfully reduced the severity of SARS-CoV-2 infection. These results were consistent with prevalent SARS-CoV-2 variants.

These results prompted researchers to test the relationship between membrane-bound mucin and SARS-CoV-2 in vivo. When Biering etc. Comparing mice with an inactivated mucin gene to mice with a normally functioning gene, we found that mice with an inactivated mucin gene contained much higher levels of viral infection in their lung tissue. understood.

But how did mucin protect against SARS-CoV-2? Since only membrane-bound mucin affected SARS-CoV-2 infection, Biering et al. I hypothesized that it would somehow block entry into the cell membrane. Surprisingly, after examining the interaction between SARS-CoV-2 and mucin using microscopic imaging techniques, researchers found that cells containing overexpressed mucin actually inhibited virus entry. Did.

Further research is needed to determine whether the interaction between mucin and SARS-CoV-2 is consistent in humans. However, the results of this study are promising and may lead to new effective treatments that may reduce the severity of SARS-CoV-2 infection.