SARS-CoV-2, the coronavirus that causes COVID-19, has been labeled with a variety of different adjectives over the past few months. Deadly, awful, and evil, just to name a few. Now, according to a new study from the University of Texas Health Science Center San Antonio, another descriptor can be added to the coronavirus’ modus operandi: deceitful.
It’s common knowledge at this point that the coronavirus is super contagious and capable of quickly infecting people through a variety of avenues (aerosol droplets, contaminated surfaces, etc). One of the factors that make SARS-CoV-2 so adept at infecting new hosts is its astounding ability to infect new cells without setting off an immune system reaction.
Now, the research team behind this study has discovered how the coronavirus is capable of evading immune system detection. SARS-CoV-2 actually disguises itself in a form of genetic camouflage. Like a cat burglar who knows the alarm code to the local jewelry store, the coronavirus tricks healthy cells into willingly allowing it access.
How is this possible? Let’s get technical for a moment. SARS-CoV-2 produces a certain enzyme called nsp16. After creating nsp16, the coronavirus uses it to “modify” its messenger RNA cap. In essence, healthy human cells are tricked into believing the coronavirus is part of themselves.
For reference, messenger RNA can be understood as the “delivery carriers” of genetic code to protein-producing ribosomes.
“It’s a camouflage,” explains lead study author Dr. Yogesh Gupta in a university release. “Because of the modifications, which fool the cell, the resulting viral messenger RNA is now considered as part of the cell’s own code and not foreign.”
The importance of this study can’t be overstated. First of all, these findings represent a big step forward in humanity’s overall understanding of how SARS-CoV-2 operates and spreads. Besides that, though, Dr. Gupta and his team believe new types of COVID-19 medications can now begin to be designed and eventually developed.
Now that the 3D structure of nsp16 has been fully mapped out, it’s possible to start designing new antiviral coronavirus drugs. These medications won’t just be limited to COVID-19 either; nsp16-blocking drugs should prove effective against future coronavirus strains as well.
These potential new drugs, in theory, will inhibit nsp16 from modifying a coronavirus’ messenger RNA cap. Consequently, one’s immune system would be able to immediately recognize a coronavirus as a foreign threat and attack it.
“Yogesh’s work discovered the 3D structure of a key enzyme of the COVID-19 virus required for its replication and found a pocket in it that can be targeted to inhibit that enzyme. This is a fundamental advance in our understanding of the virus,” says study co-author Robert Hromas, MD, professor, and dean of the Long School of Medicine.
Finally, this research serves as an upbeat reminder that as more time goes by and we continue to learn more and more about how SARS-CoV-2 functions, all that expanded knowledge will almost assuredly open the door for new ways to fight and do away with the coronavirus.
The full study can be found here, published in Nature Communications.