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Remdesivir: ‘Very potent inhibitor’ of SARS-CoV-2?

Byindianadmin

Apr 15, 2020
Remdesivir: ‘Very potent inhibitor’ of SARS-CoV-2?

Experimental Ebola drug remdesivir could stop SARS-CoV-2 from replicating by acting on a key enzyme, according to a new study from the University of Alberta.

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New evidence from an in vitro study supports the notion that remdesivir may be effective against SARS-CoV-2.

Last month, the World Health Organization (WHO) announced the launch of a multinational trial, testing the four most promising therapeutic avenues for COVID-19.

One of these avenues is remdesivir, a drug that research scientists initially developed for the treatment of Ebola, but which has recently shown some promise in fighting coronaviruses.

Following on from this evidence, and reports that the drug may have helped some patients seeking treatment for COVID-19 to recover, scientists have been studying remdesivir’s effects on SARS-CoV-2.

Stay informed with live updates on the current COVID-19 outbreak and visit our coronavirus hub for more advice on prevention and treatment.

Most recently, a team of investigators from the University of Alberta in Edmonton, Canada, has conducted an in vitro study to see if remdesivir would act on SARS-CoV-2 in the same way that it appears to act on SARS-CoV and MERS-CoV.

The researchers report their findings in the Journal of Biological Chemistry.

Last year, University of Alberta researchers showed that remdesivir could stop MERS-CoV in its tracks by interfering with the mechanism that allows the virus to replicate and spread.

“We were optimistic that we would see the same results against the SARS-CoV-2 virus,” says Prof. Matthias Götte, who contributed to both studies.

In the new study, the researchers expressed RNA-dependent RNA polymerases present in SARS-CoV and SARS-CoV-2 in insect cells. These polymerases are enzymes that allow each of the two coronaviruses to replicate.

They then exposed the enzymes to remdesivir and observed what happened. The researchers saw that the drug effectively acted on the two viruses’ polymerases i

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