Glycyrrhizin (20 beta-carboxy-11-oxo-30-norolean-12-en-3 beta-yl-2-O-beta-D-glucopyranuronosyl-alpha-D-glucopyranosiduronic acid) improves the resistance of thermally injured mice to opportunistic infection of herpes simplex virus type 1.

The effect of glycyrrhizin (GR) on the resistance of thermally injured mice to opportunistic herpes simplex virus type 1 (HSV) infection was investigated. We have previously reported that the susceptibility of thermally injured mice or normal mice inoculated with T6S cells (a clone of burn-associated CD8+ CD11b+ TCR gamma/delta + type-2 suppressor T cells), to HSV infection was about 100 times greater than it was in normal mice. When thermally injured mice were treated i.p. with a 10 mg/kg dose of GR 2 and 4 days after infection of HSV, the resistance of these mice to HSV was improved to levels observed in normal mice. The adoptive transfer of splenic mononuclear cells (MNC) from normal mice treated with GR (GR-MNC) to thermally injured mice (recipients) resulted in the improved resistance of recipients to HSV infection. Normal mice inoculated with T6S cells and exposed to HSV had an 80% mortality rate, when given GR-MNC they had a 95% survival rate. The suppressor cell activity of T6S cells was clearly counteracted by GR-MNC in vitro in a mixed lymphocyte-tumor cell reaction. The type of cells responsible for anti-suppressor cells in GR-MNC was shown to be a CD4+ CD28+ TCR alpha/beta + Vicia villosa lectin-adherent T cell. These results suggest that GR may reverse the increased susceptibility of thermally injured mice to HSV infection through the induction of CD4+ contrasuppressor T cells.