A new study by a Johns Hopkins Medicine led research team and published in the Frontiers in Microbiology journal, has found that a promising anti-cancer drug may also work as COVID-19 antiviral therapy.
This method employs a tiny molecule inhibitor known as RK-33 in order to block the virus’ ability to take over a cell’s “genetic manufacturing plant” and then make copies of itself.
Venu Raman, the study’s senior author, explains that “To date, COVID 19 vaccines have relied on just preventing the binding of a SARS-CoV-2 surface protein — known as the spike protein — to host cells and therefore enabling infection, but if the spike protein changes with new variants, the vaccine’s effectiveness may be weakened. In contrast, our research shows that RK-33’s antiviral capability is unaffected by spike protein mutations and remains consistent across 4 SARS-CoV-2 variants.”
Raman and colleagues have been looking into the protein DDX3 for years, studying its impact on cancer.
This protein is an RNA helicase, unwinding the double stranded RNA that controls many tumor cells, allowing its genetic code to be translated or read and leading to the creation of new cancer cells and the malignant spread of the illness.
Now, the team of scientists is suggesting that RK-33, a DDX3 inhibitor that has been developed in their lab, is able to slow down the progression of cancer cells by keeping the RNA from unwinding for translation.
As a result, it not only shows great promise in fighting cancer but seems to also function as a general antiviral agent!
Raman says that “We know that many RNA viruses usurp the DDX3 helicase function of the host cell to facilitate their own replication. When scientific studies revealed that even small concentrations of RK-33 blocked replication and limited infectivity by human parainfluenza type 3 virus, dengue virus, RSV, Zika virus and West Nile virus — and potentially, even HIV — our team decided to also see whether RK-33 could work on SARS-CoV-2 as well.”
In lab tests, the team used RK-33 to target DDX3 in cells infected with 4 SARS-CoV-2 variants and found that it “showed significant reductions in the viral load as much as a thousandfold. Consistent with this finding, we saw a reduction in production of most SARS-CoV-2 proteins and genes, including the protein transmembrane serine protease 2 which we know strongly participates in the infectivity and the spread of coronaviruses.”
Raman and the rest of his team members are further looking into RK-33 as an antiviral against the omicron variant – the dominant strand at the moment – and hope to have enough data to publish their results later this year.