Written by Eugenia Yi
Illustrated by Jerrie Feng
We’ve all had a cold at least once, with the average person getting it 2 to 3 times a year! We can drink all the orange juice we want and constantly suck on a cough drop, but the symptoms still usually last for at least a week. The common cold is usually caused by a rhinovirus, a type of virus that belongs to the enterovirus family; the common cold might be mosty harmless but enterovirus infections can be incredibly dangerous to people with severe asthma and could even lead to paralysis. But what if there was a cure for the common cold? Recently, researchers at Stanford University have found that mice who lack a certain protein are immune to the common cold! Usually when you get a cold, the virus enters your body and inserts a type of genetic information called RNA—similar to DNA—into the cell, which forces the cell to produce more viruses. But without this specific protein, SETD3, the cold virus can’t multiply and infect other cells.
The Stanford researchers were looking for a way to prevent enteroviruses from multiplying in cells and they accomplished this by using CRISPR, a DNA-editing tool, on healthy lung cells to remove specific protein genes in cells. The cells were then infected with 2 types of enteroviruses: one which causes a disease that affects the spinal cord and another that worsens asthma. The results showed that the protein SETD3 is vital for these viruses to infect the cells and they confirmed this by creating more human cells without SETD3 and trying to infect them enteroviruses. This experiment showed the same results, confirming that the viruses can’t replicate without SETD3!
To see if SETD3 would prevent infection in animals they observed mice born without the SETD3 gene. Before this study, SETD3 was thought to be involved in muscle contraction the researchers were concerned removing SETD3 would harm the mice, but that didn’t seem to be the case. These mice became healthy adults that were also immune to the two enteroviruses they were infected with. The mice seemed completely normal except when giving birth because without the SETD3 protein, the mouse’s muscles couldn’t contract properly to push out a baby.
However, the part of the SETD3 protein that allows cold viruses to multiply is different compared to the part that’s important for muscle contraction. This gives researchers hope that SETD3 can be used to combat enteroviruses without disturbing its regular function.
The researchers are still uncertain about how the SETD3 protein is involved in viral replication or how deleting SETD3 in humans would affect us. More research is needed to create drugs that will stop the enterovirus from helping cold viruses multiply. These drugs will also need to be engineered so that the virus can‘t become resistant to them. This discovery brings us one step closer to curing the common cold.