Herpes simplex virus type 2 regulates the IFN-gamma receptor expression and function

Abstract

This study shows that HSV-2 can cause down-regulation in IFN-gammaR expression on the monocyte surface in both HSV-2 seropositive and seronegative patients. The objective of this work is to examine and explain the mechanisms involved in the viral down-regulation of IFN-gammaR. The first question I tried to answer was whether humoral factors might participate in this down-regulation. Humoral factors were not involved in this phenomenon. Next, cell-to-cell interactions were examined. T, B or natural killer cell depletion experiments were conducted in peripheral blood mononuclear cells of both HSV2 seropositive and seronegative patients. The results suggest that NK cells and T cells but not B cells were involved in the IFN-gammaR downregulation in HSV-2 seropositive patients. In addition, purified monocytes also demonstrated IFN-gammaR down-regulation after HSV-2 exposure in seropositive patients. I concluded that, in HSV-2 seropositive patients, NK cells may have an inhibitory effect and T cells may have a facilitatory role in the down-regulation of IFN-gammaR. (Abstract shortened by UMI.)