University of Texas at Austin research sheds light on remdesivir

New research from the University of Texas at Austin sheds new light on the antiviral drug Remdesivir COVID-19 and could lead to more effective antiviral treatments. The study was published today in the journal Molecular Cell.

Remdesivir is the only treatment of its kind currently approved for the coronavirus in the United States. It targets a part of the coronavirus that allows it to make copies of itself and spread throughout the body.

For the first time, scientists identified a critical mechanism that the drug uses and discovered information that drug companies can use to develop new and improved antivirals to use the same trick. According to co-author Kenneth Johnson, the finding could also lead to more effective drugs, which means a patient could take less dose, see fewer side effects, and experience faster relief.

Vials with the drug Remdesivir lie amidships during a press conference on the start of a study with the Ebola drug Remdesivir in particularly seriously ill patients at the Eppendorf University Medical Center (UKE) in Hamburg on April 8, 2020

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“Right now it’s a five-day program that uses quite a bit of remdesivir,” Johnson, professor of molecular life sciences at UT Austin, said in a press release. “It’s inconvenient and has side effects. What if you could just take one pill and that was all you had to do? It would make a big difference in the here and now.”

Study co-author David Taylor likened the trick the team identified to a paper jam in the virus’ photocopier. Remdesivir turns off this photocopier called RNA polymerase by preventing the virus from copying the genetic code and its ability to make duplicates and spread throughout the body. The team realized where the drug was able to glue the gears together and bring the machine to a standstill.

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Baylor Scott & White Talks About Remdesivir Study

We talk a lot about the devastating effects of COVID-19 … but there is some good news to report. The drug Remdesivir has had positive results. Dr. Robert Gottlieb, principal investigator for the Gilead-published Remdesivir study, spoke to Casey Claiborne of Good Day Austin on Saturday morning about the importance of these positive results.

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“We were able to identify the point where this jam occurs,” said Taylor, assistant professor of molecular life sciences. “We now know exactly what is creating this block. If we want to make the block even worse, we can do so.”

The team has recreated the process in a laboratory tray that takes place in a patient infected with SARS-CoV-2 who is then given remdesivir. In a scientific first, the scientists developed a method to produce fully functional RNA polymerases to copy the viral genetic material. Next, they added some form of remdesivir.

While the drug was doing its job, the researchers paused the process immediately after the reaction with remdesivir was complete (15-20 seconds) and took a 3D snapshot of the molecules in exquisite detail using a cryo-electron microscope at UT Austin’s Sauer Structural Biology Laboratory. The image enabled them to reconstruct exactly how Remdesivir shortens the copying process.

Johnson said SARS-CoV-2 is the third coronavirus to make the leap from animals to humans in less than 20 years. Even if this pandemic is brought under control soon, it still makes sense to continue developing weapons against coronaviruses. He says the search for more effective antivirals could soon become more urgent as new strains of SARS-CoV-2, the virus that causes COVID-19, keep popping up.

“We may need other drugs that work like remdesivir but are so different that they can target the mutated forms,” ​​said Johnson. “It’s like having a backup system, like an emergency parachute in case the main shaft doesn’t work.”

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The version of the paper released today is a pre-proof, which means it has been accepted for publication and peer-reviewed, but has not yet been fully formatted for final publication. It is currently planned to appear in a print edition of the magazine in April.

The study is coauthored by postdoctoral fellow Jack Bravo and PhD student Tyler Dangerfield.

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