When applying the drug benfooxythiamine, an inhibitor of this pathway, SARS-CoV-2 replication was suppressed and infected cells did not produce coronaviruses.
Canterbury: Researchers during a recent study identified a potential new treatment that suppresses the replication of SARS-CoV-2, the virus that causes COVID-19. In order to multiply, all viruses, including coronaviruses, infect cells and reprogramme them to produce novel viruses. The study `Targeting the pentose phosphate pathway for SARS-CoV-2 therapy` has been published by the scientific journal Metabolite.
The research revealed that cells infected with SARS-CoV-2 can only produce novel coronaviruses when their metabolic pentose phosphate pathway is activated.
When applying the drug benfooxythiamine, an inhibitor of this pathway, SARS-CoV-2 replication was suppressed and infected cells did not produce coronaviruses.
The research from the University of Kent`s School of Biosciences and the Institute of Medical Virology at Goethe-University, Frankfurt am Main, found the drug also increased the antiviral activity of `2-deoxy-D-glucose`; a drug which modifies the host cell`s metabolism to reduce virus multiplication.
This shows that pentose phosphate pathway inhibitors like benfooxythiamine are a potential new treatment option for COVID-19, both on their own and in combination with other treatments.
Additionally, Benfooxythiamin`s antiviral mechanism differs from that of other COVID-19 drugs such as remdesivir and molnupiravir. Therefore, viruses resistant to these may be sensitive to benfooxythiamin.
Professor Martin Michaelis, University of Kent, said, “This is a breakthrough in the research of COVID-19 treatment. Since resistance development is a big problem in the treatment of viral diseases, having therapies that use different targets is very important and provides further hope for developing the most effective treatments for COVID-19.”
“Targeting virus-induced changes in the host cell metabolism is an attractive way to interfere specifically with the virus replication process,” added Professor Jindrich Cinatl from Goethe-University Frankfurt
