[Therapy of banal HSV lesions: molecular mechanisms of the antiviral activity of zinc sulfate].

Preparations of heparin in combination with the physiologically harmless and even beneficial zinc sulphate are available for the topical treatment of superficial mucocutaneous lesions caused by HSV (herpes simplex virus). We study the molecular mechanism of the antiviral effects of zinc ions. A concentration of 100 mumol/l Zn2+ in the culture medium reduces the virus yield in a HSV infected AGMK cell line to less than 1/1000 of the control. At this concentration zinc sulphate does not exert any major cytotoxic effects, nor does it block the synthesis of viral or cellular DNA. Free virus, however, is inactivated by 8 orders of magnitude by 15 mmol/l zinc sulphate within a few hours. The inactivated virus is limited in the glycoprotein-dependent functions adsorption and penetration. Electron micrographs show massive deposition of zinc onto virion components. The dramatic antiviral effect in vivo is therefore explained by an inhibition of virion glycoprotein functions after accumulation of zinc in the virion, presumably by binding to sulphhydryl groups of glycoprotein B.