Science News takes rhinovirus by the (one) horn with a study that finds a weak spot in the way the germ spreads inside our cells:
Researchers have identified a key protein in humans that some viruses use to multiply inside of human cells. Disabling that protein, instead of attacking the virus itself, may prevent infections from spreading. In mice and human cells engineered to lack this protein, the viruses couldn’t replicate, Jan Carette, a microbiologist at Stanford University School of Medicine, and colleagues report September 16 in Nature Microbiology.
Using the gene-editing tool CRISPR, Carette and colleagues systematically deleted chunks of DNA to build a library of human cells, each missing one gene and therefore unable to make that gene’s corresponding protein. The researchers then infected the cells with two types of viruses, one that causes colds and another that has been linked to neurological diseases.
Using different viral proteins like hooks, the scientists pulled out human proteins that were physically attached to a viral protein. That let the team identify which human proteins were interacting with viral ones — an indication that the virus was using that protein to hijack the cell.
One human protein was repeatedly fished out of the cells: SETD3. And experiments indicated that the viruses needed SETD3 to take over the cell. Scientists knew this protein could affect actin proteins, which help muscles contract. But its role in viral infections came as a surprise.
When the researchers injected viruses into mice engineered to lack a working version of the SETD3 gene, the mice didn’t get sick. Human lung cells that also lacked the gene remained healthy. (Lung cells are often used in these types of studies because they are especially susceptible to many rhinoviruses that cause colds.)
Repeating those experiments with similar but potentially more serious viruses suggested the approach may be effective against more than just the common cold. Engineered human cells didn’t become infected when they were exposed to viruses that cause hand, foot and mouth disease and a polio-like spinal cord disease called acute flaccid myelitis.
Scientists don’t fully understand what this gene does in the human body, and getting rid of it completely could have unknown effects, says Vincent Racaniello, a virologist at Columbia University who wasn’t involved in the work. “The authors show that mice lacking the gene for SETD3 are viable and resistant to infection. However, this observation does not mean that SETD3 in humans is dispensable,” he wrote in an e-mail.