The intracellular redox state is maintained in its physiological reduced conditions by several molecular factors, among which glutathione (GSH) represents, the most abundant intracellular thiol with antioxidant functions.

In this article, we have summarized results, obtained in our laboratories over the last few years, demonstrating that during viral infection, an imbalance in the intracellular redox state is induced by different viruses both in in vivo and in vitro experimental systems, via a decrease in GSH levels. The oxidative environment induced by viruses or by other pro-oxidant agents, participates in the development of infection, either by increasing viral replication itself or by activating the inflammatory responses to infection. We have seen that the administration of reduced glutathione to infected cells restores the intracellular redox state and inhibited replication of parainfluenza, Herpes Simplex 1 and immunodeficiency virus in vitro.

In vivo studies, we found that GSH also exerts an antiviral activity and inhibits the progression of the disease in a murine model of AIDS (systemic administration) and in Herpes Simplex-induced keratitis in rabbits (topical administration).

Overall data demonstrate that, among the mechanisms regulating virus/cell host interactions, the intracellular redox state could play a key role in controlling viral replication, cellular response to infection and progression of the disease.