Lab led by researcher Blanton Tolbert partners with international scientists, seeks expanded NIH support to “target virus at molecular level”
A team of scientists, including Blanton Tolbert, associate professor in the Department of Chemistry at Case Western Reserve University, and his research lab, are conducting the underlying research to develop an antiviral to slow the spread of the novel coronavirus that causes COVID-19.
Tolbert said he and research partners from Duke and Rutgers universities
hope to hear soon from the National
Institutes of Health (NIH) whether their project to develop an antiviral against
the novel coronavirus behind the global pandemic of COVID-19 will receive
The research team recently laid the groundwork to develop
novel antivirals against Enterovirus 71 (EV71), a similar RNA virus that causes hand, foot
and mouth disease. Tolbert said they are now poised to make
significant inroads into identifying vulnerable COVID-19 targets.
“We’ve already shown the necessary ‘proof of concept’ with
EV71, which shows we know how to get things done,” Tolbert said. “And now we
have assembled an expanded international group to include scientists from the
University of Michigan, the United Kingdom and Taiwan, where they isolated some
very early COVID-19 viruses from two infected patients at Chang Gung Memorial Hospital.”
Tolbert said that his Taiwanese collaborators have been able
to clone the novel coronavirus in the lab, providing a copy to study at the
molecular level—the first step in learning how it works.
lab studies basic biochemical processes of ribonucleic acid (RNA) viruses,
working to better understand the physical interactions between the virus and
host. Their most recent work has determined the 3D structures of pieces of
viruses from HIV and EV71, he said.
While EV71 is not a coronavirus, both fall under “the bigger
umbrella of positive-sense RNA viruses that infect humans,” he said.
“And if you can figure out how the virus interacts with the cellular
environment it has infected, where the real activity takes place, you can
understand it better,” Tolbert said. “You can look at how it takes over the
cellular machinery with the ultimate goal of making drugs to block those
processes. But first you have to know how it hijacked the cells in the first
Early start on coronavirus focus
It was still early February of this year when Tolbert sat in a conference room in Durham, North Carolina, with colleagues from Rutgers and host Duke University. They were meeting to celebrate their recent success with EV71 and to talk about next steps in publishing (their work is published on a pre-print site, but not yet in a named journal) and expanding their work on that particular virus.
But a new, still barely known novel virus, which had just appeared
in Wuhan, China, was also on their minds.
So when Tolbert and his colleagues turned their attention and
expertise toward COVID-19, they were ahead of the curve, he said. The NIH
didn’t even announce for another two weeks that emergency funds to fight
COVID-19 were available.
“We were already working on something for which there are no antivirals, something with high mortality and morbidity (illness and other conditions associated with the virus) rates—especially for children in Southeast Asia,” he said. “So when we saw the early signs that this coronavirus had no antivirals or vaccine, we decided to see how we might get involved, knowing we already had that proof-of-concept with this other virus.”
He said how quickly the research group hears from the NIH on
whether it will get a new influx of funding to tackle COVID-19 will likely
depend on whether the agency considers the work urgent enough—either for
“flattening the curve,” the phrase for leveling out over time the rapidly rising
number of cases, or finding a permanent antiviral.
cannot anticipate what is coming next,” he said. “This is something that needs
to be done if an antiviral is going to be achieved. The bottom line is that we believe we are equipped and ready to go, and
we can make a difference.
“I don’t know if that means it will lead directly to an antiviral yet, but I believe we can find ways to target this at the molecular level.”