The University of Texas Southwestern Medical Center has found a crucial gene that is involved in our body’s natural process of destroying viruses. Manipulating this gene can lead to the creation of many treatments for a wide range of viral infections, even COVID-19. Ph.D., Xiaonan Dong, and his team began with observing human cells infected by a variety of viruses and examining over 18,000 genes in order to find the effect they may have on autophagy.
What is Autophagy?
Autophagy is our cells’ process of recycling damaged parts by breaking them down and using them as “building blocks” to create new components. However, it degrades more than just defective cells. Autophagy is also known to destroy bacteria and viruses that can cause infection.
In this diagram, the unwanted material, such as dysfunctional organelles, is isolated into the autophagosome. Then, the autophagosome is fused with single-layered vesicles called lysosomes which degrade and recycle the cellular garbage.
First, the team began with herpes simplex virus type 1 or HSV-1 and Sindbis virus. HSV-1 is a common and contagious virus known for causing sexually transmitted diseases as well as cold sores. Meanwhile, the mosquito-transmitted Sindbis virus causes rash, headache, and joint pain. From these two viruses, researchers found 216 genes that played a role in viral autophagy. In order to reveal the genes that had the most influence on autophagy, they analyzed the processes that these genes regulated through a method of bioinformatics. Bioinformatics is a method of studying biological data such as DNA and amino acid sequences with the assistance of computer science.
Soon after, Dong and his colleagues discovered a gene named sorting nexin 5 or SNX5 which performed a recycling action similar to autophagy. Viruses typically enter cells through this specific pathway, so researchers made the hypothesis that SNX5 is a key player in autophagy. In order to confirm this, they deactivated SNX5 in their experiment with the human cells. Consequently, the cells were much more inefficient when performing autophagy on HSV-1 and Sindbis viruses. Meanwhile, autophagy to recycle dysfunctional cells and remove bacteria was activated, showing the same results as the control group. This suggested that SNX5 was a gene that specifically aided viral autophagy.
The research team experimented with many other viruses such as influenza A, West Nile, and poliovirus. In all of these trials, the results had suggested that SNX5 was a crucial component in our body’s defense mechanism against viruses. Furthermore, canceling SNX5 showed an increase in susceptibility to viral infection for both human cells and animal cells.
With Dong’s identification of SNX5 is a crucial gene in viral autophagy, scientists can potentially manipulate SNX5 and find new methods of fighting off viruses. Today, we treat viruses by studying their individual weaknesses, meaning that every virus requires a different approach. Dr. Dong explains that by better understanding the way our body naturally degrades viruses, we can create a “more general strategy for developing broad-spectrum antiviral therapeutics that combat an array of different viral infections.” With our newfound knowledge of SNX5 in viral autophagy, we can take the next step in medicine by improving our immune systems.
Kyle Phong, Youth Medical Journal 2021
Nature, “Sorting nexin 5 mediates virus-induced autophagy and immunity, 16 December 2020,
News Medical Life Sciences, “Researchers identify key gene necessary for cells to consume and destroy viruses”, 17 December 2020,
UT Southwestern Medical Center, “Giving cells an appetite for viruses”, 16 December 2020
National Cancer Institute, “Autophagy”
National Human Genome Research Institute, “Bioinformatics”