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Gazzetta Medica Italiana - Archivio per le Scienze Mediche 2019 October;178(10):792-8

DOI: 10.23736/S0393-3660.18.03964-5

Copyright © 2018 EDIZIONI MINERVA MEDICA

lingua: Inglese

Antiviral activity and possible site of action of zinc against Hepatitis C virus in vitro

Arash SHAKIBZADEH 1, Jamal SARVARI 2, Farzaneh SABAHI 1 , Mehrdad RAVANSHAD 1

1 Department of Virology, School of Medical Science, Tarbiat Modares University, Tehran, Iran; 2 Department of Bacteriology and Virology, Shiraz University of Medical Sciences, Shiraz, Iran



BACKGROUND: Treatment of hepatitis C virus (HCV) infection has always been a matter of concern. Finding a cost-effective compound with an anti HCV activity and with minimum side effects could advance HCV therapy. On the other hand, it has been revealed that increasing intracellular zinc concentration has the potency to inhibit and impaired certain viruses.
METHODS: In order to analyze antiviral activity of zinc on HCV and find out the possible mode of action, different concentrations (10, 50, 100 and 200 µM) of zinc sulfate (ZnSO4) was evaluated against different stages of HCV JFH1 life cycle in Huh7.5 cells in vitro. Antiviral activity of zinc salt in pre, simultaneous and post infection treatments were estimated by quantitative RT-PCR and controlled by mock control and MgSo4 as salt control. Cytotoxicity of different doses of ZnSO4 on cells was assessed using MTT assay.
RESULTS: ZnSo4 markedly inhibited HCV replication in post adsorption phase compare to the mock control and salt control in a dose dependent manner. Increasing ZnSO4 concentrations (10, 50, 100 and 200 µM) decreased HCV RNA levels by 6.2%, 7.68%, 9.54% and 13.7% respectively in post infection treatments.
CONCLUSIONS: In this study we demonstrate that ZnSO4 possesses antiviral activity against HCV, beside the site of action of the zinc is the replication stage of HCV life cycle with probable effect on HCV RNA polymerase. Results from this study nominate zinc as a potent adjunct or anti HCV component for HCV therapy.


KEY WORDS: Immunologic cytotoxicity; Hepacivirus; Pharmacology

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