The current COVID-19 vaccines being distributed around the country instruct the body on how to fight the coronavirus’ key proteins in advance of an infection. But with SARS-CoV-2 mutating in some alarming ways around the world, researchers are worried about the possibility of viral escape: the virus mutating enough that it is able to evade antibodies and, in a worst-case scenario, even vaccines. That means that finding alternate weapons and avenues of attack against COVID-19 remains crucial, especially amid growing speculation that it will become a recurring blight. Now, researchers at Ohio University have leveraged the university’s in-house supercomputing power to probe another possible weak point of the deadly virus: its RNA, which allows it to reproduce.
“We are studying a section of RNA that does not code for proteins and is found in the coronavirus causing COVID-19 and other similar viruses,” explained Jennifer Hines, a professor of chemistry and biochemistry at Ohio University. “We are comparing it with the viral RNA from the SARS outbreak nearly 20 years ago and looking for a possible target for an antiviral drug that can attack the virus and stop it from reproducing. We are looking for the Achilles’ heel of the COVID-19 virus.”
Specifically, the researchers were interested in learning more about one section of the viral RNA. “[This section] is highly conserved in the COVID-19 virus,” Hines said, “meaning that while other parts of the virus continue to evolve, this part of the virus is normally like a rock. And for the virus to cause disease, it needs to keep replicating inside the human body. So we are looking at this section of the RNA as a possible target for an antiviral.”
To hunt for this heel, the researchers used the supercomputing resources at the Ohio Supercomputer Center (OSC): specifically, the Owens cluster, named after famed athlete Jesse Owens. Owens’ 824 nodes include 648 Intel Xeon Broadwell-based compute nodes, 160 GPU-powered nodes with Nvidia Tesla P100s and 16 nodes with extra memory. All-in-all, Owens boasts around 750 peak teraflops of performance.
Hines and her colleagues used the Owens cluster – to which they were awarded free priority access – to examine differences in this key section of RNA between SARS and COVID-19. Based on those results, the team then progressed to lab-based research.
“Using complementary biochemical and computational methods, we determined that the structural flexibility of this important noncoding RNA motif differs compared to that in the early 2000s SARS-CoV outbreak by only a single nucleotide change,” Hines said. “We also identified FDA-approved drugs that bind the RNA motif and alter its flexibility. This was an exciting observation since the structure and flexibility of noncoding RNA affects its function, indicating that it may be possible to develop antiviral therapeutics that specifically target this RNA motif and disrupt its function.”
To read the paper, which was published in Biochemical and Biophysical Research Communications, click here.