Existing Drugs May Inhibit SARS-CoV-2 Virus

CHANGSHA, China - July 26, 2021 - PRLog -- In a recent study published in Nature Communications Biology, researchers from the U.S. Department of Energy's (DOE) Argonne National Laboratory and the University of Chicago identified a way to interfere with a sneaky mechanism the virus uses to prevent a response from an infected person's immune system.

This new weapon against COVID-19 actually comes from the fight against cancer, as scientists have found that tipiracil, a drug used to treat colorectal cancer, can inhibit the action of one of the main proteins that make up SARS-CoV-2.

SARS-Cov-2 is a ribonucleic acid (RNA) virus. RNA is a type of genetic code that can be translated into proteins that allow the virus to replicate. During its RNA duplication, the virus would typically have a distinct chemical genetic signature -; a string of molecules, or bases, that appends to one end of SARS-CoV-2's RNA backbone.

This chemical signature would normally be recognizable by the body and produce an immune response, but the virus has a special way of hiding the extra molecules and sneaking into the body undetected. The research team used the resources of the Advanced Photon Source (APS), a DOE Office of Science User Facility at Argonne, to test a new treatment option that may foil this mechanism.

The research was led by Andrzej Joachimiak of Argonne and the University of Chicago, with Argonne protein crystallographer Youngchang Kim and University of Chicago structural biologist Natalia Maltseva and their colleagues. Joachimiak is the director of the Structural Biology Center (SBC) at the APS, and the research team used the high-powered X-ray beams generated there to study one of the virus's proteins, called Nsp15.

This protein acts like a molecular scissors, cutting regions of the virus that are involved in its ability to make copies of itself. As more and more of those strings of molecules -; made up of uridine, one of the main components of nucleic acid -; are produced, the Nsp15 molecule removes them, essentially giving the virus the haircut it needs to pass undetected undercover.

The virus uses strings of uridine to duplicate itself and translate those copies into protein. Those strings of uridine would typically create an immune response, but the Nsp15 cuts it off, allowing the virus to proliferate and infection to spread. The tipiracil inhibits the action of Nsp15 by binding in the place where Nsp15 otherwise would.

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