Hormonal modulation of herpes simplex virus replication in a mouse neuroblastoma cell line

In this study, the effect of the synthetic glucocorticoid hormone dexamethasone (DXM) on HSV replication was studied in a DXM receptor-positive mouse neuroblastoma (NB) cell line. In cells treated with 10(-7) M DXM and then infected with HSV, there was a statistically significant 9-18-fold increase in the amount of virus produced in these cells compared to untreated controls. Adsorption kinetic studies with HSV were performed in DXM-treated NB cells and untreated controls. It was found that there was a significant increase in the adsorption rate of HSV in the DXM-treated cells as compared with the controls. During the course of these studies, a strain of NB cells was noted to have lost its ability to stimulate HSV replication following DXM treatment. Receptor binding assays were performed on cytosols prepared from NB cells that responded with an increase in HSV titers to DXM treatment and the new strain of NB cells that was DXM refractile. These latter cells were found to have lost their DXM receptors. These results indicate that the modulation of HSV replication of DXM treated cells was regulated by the presence of DXM receptors in these cells. Once lost, the cells do not respond to DXM treatment with increased HSV replication. These observations may lead to a clinical assay to determine patients with high glucocorticoid levels who may be at risk of recurrent herpes infections.