AbstractVarious in vitro studies have shown specific inhibition by lithium of the replication of a number of DNA virus groups (herpes-, pox- and adenoviruses) at concentrations which do not affect normal cell functions. There is less agreement on RNA viruses; two RNA virus groups (picorna- and orthmyxo-viruses) are not inhibited by lithium, while inhibition of paramyxo-viruses has been reported. The effect on human immunodeficiency virus (HIV) requires further study. Concentrations of lithium affecting uninfected cell growth and division are influenced by the cell type, but are at higher levels than those which inhibit virus replication. Viral DNA replication is a major target of inhibition of herpes viruses; the effect on viral proteins is consistent with this, demonstrating reduced synthesis of the late structural proteins which are dependent on DNA replication. Lithium may act on the viral enzyme DNA polymerase via competition with potassium. Mutants resistant to lithium have been isolated which should enable these results to be confirmed. Potentially clinically important is a synergistic interaction between lithium and certain nucleoside analogues capable of chain termination. In vivo studies on lithium have consistently shown a reduction in frequency of recurrence and severity of labial herpes infections following oral lithium. Topical treatment with lithium succinate ointment has reduced the number of herpetic lesions in an animal model while in human subjects early treatment of recurrent lesions reduced pain, virus excretion, and time to healing. Further clinical studies should aim to enhance skin penetration of lithium, perhaps coupled to a nucleoside analogue capable of synergistic interaction.
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