Rachel Roberts
11/4/19
Bates, Sofie. “Disabling One Protein Might One Day Lead to a Cure for the Common Cold.”
Science News, 23 Sept. 2019,
For Current Event 7, I decided to review Sofia Bates’ article, “Disabling One Protein Might One Day Lead to a Cure for the Common Cold.” She begins by stating that researchers have found a key protein in humans that viruses use to multiply inside of human cells. If scientists can disable this protein, it could prevent the spreading of infections. According to Jan Carette, a microbiologist at Stanford University School of Medicine, when the protein is disabled in mice and human cells, the virus could not replicate. Ellen Foxman, an immunologist at Yale School of Medicine, says that “It’s not quite a cure for the common cold, but it’s an interesting step forward.” Carette and her collages used CRISPR, the gene-editing device to identify and pull out the human proteins that were attached to viral proteins. They found that the protein SETD3 was repeatedly pulled out. They also found that when SETD3 was taken out of mice, they would not become sick. These discoveries gave scientists the idea to remove the protein. However, there isn’t enough known about it and the effects of removing it for the procedure to be safe. For example, Vincent Racaniello, a virologist at Columbia University, said, “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,” This uncertainty caused for the idea of drugs that could block proteins and their viral counterparts from interacting or drugs that would destroy proteins interacting with viral ones. The discovery of how specific proteins help viruses multiply could help create a cure for the common cold and many other viral infections.
While the research of SETD3 has been mainly focused on curing the common cold, its removal could also help cure other viral infections. In her article, Bates wrote, “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. And when mice were exposed to these viruses, the rodents that didn’t have a functioning version of SETD3 were much more likely to survive than those that had the working gene.” This quote shows how the removal of SETD3 helped the mice recover from other illnesses. This means that scientists can use similar methods to find cures to other diseases, increasing the length and quality of life.
When reading this article, I found that there were many good aspects of her writing. She was able to explain the information used in the article very well, especially since I did not know much about the subject before reading it. For example, her explanation of how the scientists used CRISPR was helpful, and it allowed me to explain it in this review. Also, while there was not much of a background story following the person who made the discovery, Bates was still able to make the article very interesting by creating the storyline of how the scientists discovered SETD3. Although the story was captivating, there were some choppy areas of the article. It transitioned quickly between topics, which would sometimes confuse me. For example, the article went from the article went discovery of the key proteins, to the statistics of the common cold, and then back to how the proteins were identified. While the statistics helped understand the issues of finding the cure to the common cold, it felt slightly misplaced in the sense that it broke up the story. There were slight transitions at the end of the paragraphs, but not enough to fully cue the reader in that topics will shift. While most of the article was well written, it would be much easier to read if there was a clear order of information.
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