Ohio University Scientists Search For A Way To Shut Down Coronavirus

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ATHENS, Ohio (WOUB) — In the race to defeat COVID-19, much of the focus has been on vaccines that stimulate the body’s immune system to prepare for an attack.

But a research team at Ohio University is focused on another approach: Shut down the genetic machinery that allows the virus to replicate.

The team is led by biochemistry professor Jennifer Hines. To understand their research, it’s helpful to understand a couple of things about viruses.

Jennifer Hines
Jennifer Hines. [Courtesy of Ohio University]
First, viruses are always mutating, which makes it challenging to treat them. Each significant mutation requires a new vaccine.

However, there are parts of a virus’s genetic code that change very little, including the parts that have to do with replication.

“Viruses don’t let things stay constant unless it’s important,” Hines said, “so the structure of RNA, if it’s kept really constant, probably means that it has a very important function.”

Second, when a virus like COVID-19 enters the body, its RNA, which carries its genetic code, enters our cells. It then hijacks the machinery inside, known as ribosomes, to produce the proteins it needs to survive.

Hines and her team focused on a segment of the COVID-19 RNA. They compared it with the RNA from the coronavirus that caused the SARS outbreak in 2003, which also infected people around the world.

What they found is that this small segment of RNA in the COVID virus is almost identical to the segment in the SARS virus.

This suggests the RNA segment plays an important role in the virus’s genetic code, perhaps in replication. If that’s true, and if this RNA segment could be disrupted, that could potentially prevent the COVID virus from replicating.

Hines and her team used synthetic models of the RNA segment to see what would happen if it was exposed to a couple of powerful antiviral drugs known to dock with RNA and disrupt its function.

Their simulation showed that the drugs docked with the segment of COVID RNA and made it more flexible.


“Molecules are not static … they breathe and flex and move around and RNA especially does,” Hines said. “There is definitely a relationship between the structure and the flexibility of the RNA and the function that it plays.”

A change in flexibility could prevent the RNA from performing its function.

The encouraging findings will be published soon in a biochemical journal. But there is still a long way to go before a drug is developed to prevent the coronavirus from replicating.

Hines and her team are assuming that because of its stability, this RNA segment is involved in replication. And they’re assuming the change in flexibility will be enough to shut it down.

“Those are big assumptions,” she said.

More research will be needed to find out if these assumptions are correct. And even if they are, a drug will need to be developed that specifically targets this segment of RNA and doesn’t have any serious side effects.

This goes back to the insidious nature of viruses:  They hijack our cells and turn them against us.

“And that’s one of the reasons why it’s so difficult to target this kind of viral infection,” Hines said. “Because you can’t target the human ribosome because you need the human ribosome to make your normal regular proteins.”

Hines and her team are already working on the search for a drug. It’s a process that could take years, and by then, vaccines have hopefully long since brought COVID-19 under control.

There are other coronaviruses out there, however. And because the RNA segment that may control replication is so stable, a drug that shuts down replication might be effective in many coronavirus variants.

It might even be the elusive cure for the common cold which, yes, is caused by a coronavirus.