Title Antiviral activity of Schizonepeta tenuifolia Briquet against noroviruses via induction of antiviral interferons
Author Yee Ching Ng1, Ye Won Kim2, Jeong-Su Lee3, Sung Joon Lee2, and Moon Jung Song1*
Address 1Virus-Host Interactions Laboratory, Department of Biosystems and Biotechnology, Division of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul 02841, Republic of Korea, 2Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul 02841, Republic of Korea, 3Food Microbiology Division, Food Safety Evaluation Department, National Institute of Food and Drug Safety Evaluation, Osong 28159, Republic of Korea
Bibliography Journal of Microbiology, 56(9),683–689, 2018,
DOI 10.1007/s12275-018-8228-7
Key Words antiviral activity, norovirus, Schizonepeta tenuifolia Briquet (ST), natural phytochemicals, interferons
Abstract Human noroviruses are the causative agents of non-bacterial gastroenteritis worldwide. The rapid onset and resolution of disease symptoms suggest that innate immune responses are critical for controlling norovirus infection; however, no effective antivirals are yet available. The present study was conducted to examine the antiviral activities of Schizonepeta tenuifolia Briquet extract (STE) against noroviruses. Treatment of human norovirus replicon-bearing HG23 cells with STE at 5 and 10 mg/ml concentrations resulted in the reduction in the viral RNA levels by 77.2% and 85.9%, respectively. STE had no cytotoxic effects on HG23 cells. Treatment of RAW 264.7 cells infected with murine norovirus 1 (MNV-1), a surrogate virus of human noroviruses, with STE at 10 and 20 μg/ml concentrations resulted in the reduction of viral replication by 58.5% and 84.9%, respectively. STE treatment induced the expression of mRNAs for type I and type II interferons in HG23 cells and upregulated the transcription of interferon-β in infected RAW 264.7 cells via increased phosphorylation of interferon regulatory factor 3, a critical transcription regulator for type I interferon production. These results suggest that STE inhibits norovirus replication through the induction of antiviral interferon production during virus replication and may serve as a candidate antiviral substance for treatment against noroviruses.