New Antivirals kill SARS-CoV-2

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ISLAMABAD, APRIL 23 (Online): A study has found that newly engineered antiviral compounds can neutralize SARS-CoV-2, the virus that causes COVID-19, in human airway cells. The compounds also improved survival rates in mice infected with MERS.
Research to find an effective COVID-19 treatment is ongoing.
Corona viruses are a large group of viruses responsible for respiratory tract infections, ranging from the common cold to severe acute respiratory syndrome Although corona viruses are a familiar threat, currently no vaccines or antiviral drugs can prevent or treat the infections in people.
The ongoing COVID-19 pandemic emphasizes the need for effective treatments and drug development. Scientists are hard at work, trying to find an antiviral agent effective against 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.
Much hope has been placed in remdesivir, an antiviral drug that was originally developed as a treatment for Ebola.
However, recent clinical practice guidelines developed by an international panel give only a “weak” recommendation for the drug in patients with severe COVID-19, and one recent study suggested that seaweed extract could be more effective.
Amid the continued search for a COVID-19 treatment, new research has homed in on a group of antiviral compounds that target an essential enzyme in corona viruses.
The study’s authors report that the compounds drastically improved survival rates in a mouse model of MERS and neutralized SARS-CoV-2 in cells from people with COVID-19.
The findings appear in the journal Science Translational Medicine.
An essential protease
The research, led by scientists from Wichita State University, in Kansas, is based on the inhibition of a critical viral enzyme called 3C-like protease.

This enzyme is essential for the virus to replicate, and therefore survive, and given its crucial role, the enzyme is sometimes known simply as the “main protease.”
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