“The compound was found to significantly inhibit viral entry and infection in both, HCV-LP (in vitro) and HCV cell culture (ex vivo) systems,” the authors wrote.
The team then sought to determine how rutin worked to inhibit virus entry and discovered that the greatest protection occurred when the flavonoid was present in the cell culture medium before the virus was added.
The researchers determined that there was no protective effect once the virus-like particles had bound to the cells. Rutin also showed no benefit when researchers added and withdrew it before infection. This suggested that the flavonoid interferes with the virus’s binding step. Extremely high concentrations of rutin did not produce cellular toxicity during the testing, the team said.
According to the scientists, this discovery may expand current thinking on hepatitis C therapies. Most of today’s direct-acting antiviral drugs target the replication step of the HCV lifecycle. However, recent studies have indicated that adding entry inhibitors to these medicines has a synergistic effect on the efficiency of antiviral treatment. Furthermore, current HVC drugs are expensive and may not be well tolerated, the team said. To this end, the researchers suggest that using a combination of inhibitors that target different stages of the virus lifecycle might be a better therapeutic strategy.
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