In the treatment of SARS-CoV-2, the virus that causes COVID-19, antiviral drug remdesivir has emerged as a promising candidate
Remdesivir works by disrupting the virus’s ability to replicate, but its exact mechanism has remained a mystery.
In a new study, researchers have found just how the drug works at the molecular level.
They also found that two drugs that work in a similar manner, ribavirin and favilavir, do not bind as effectively to the virus.
The research was conducted by a team at the University of Chicago.
Remdesivir works by disrupting SARS-CoV-2’s RNA polymerase, a key enzyme that the virus needs to replicate itself.
When this enzyme is disrupted, the virus cannot multiply and spread within the body.
But in patients, the drug has produced varied results.
Some clinical trials have shown that patients who received it recovered faster and had improved mortality rates, while other trials have shown that the drug did not reduce mortality or hospitalization lengths.
Since the beginning of the pandemic, the team had been using advanced computational simulations to systematically look at the proteins that allow the virus to replicate or infect cells.
They also had looked at the key candidate drugs that are used to inhibit those processes.
In the study, the team simulated the interaction between the enzyme and three drugs meant to inhibit it: remdesivir, ribavirin, and favilavir.
They found that remdesivir binds strongly to the virus, but ribavirin and favilavir do not bind as effectively.
They also found that remdesivir destabilizes the virus’s protein complex, also reducing its ability to replicate.
The team says now that simulations show that the drug should work, scientists can focus on finding the best strategies to deliver the drug more effectively.
One author of the study is Prof. Juan de Pablo.
The study is published in the journal ACS Central Science.
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