Herpesvirus-Lymphoid Cell Interactions: Comparative Studies on the Biology of Herpes Simplex Virus-Induced Fc Receptors in B, T, and “Null” Lymphoid Cell Lines

Abstract

We have investigated the induction of Fc receptor (FcR) in different types of lymphoid cell lines (LCL) infected with herpes simplex virus (HSV). Subpopulations of certain of these LCL normally express FcR unrelated to herpetic infection. Differentiation of virus-induced FcR from that related to normal cell function was therefore possible. FcR detection was carried out by means of a rosette assay using ox erythrocytes coated with 7S immunoglobulin G (EA rosettes). Both HSV types 1 and 2 were found to induce FcR in B, T, and “null” (i.e., non-B, non-T) type LCL; however, in all the LCL tested, this HSV-induced FcR expression appeared to be more restricted in the responding T LCL than in responding B and null type LCL. In addition, kinetic experiments revealed that the time course of HSV-induced FcR expression differed among these LCL types tested. Interestingly, a number of LCL were resistant to HSV infection or restricted HSV gene expression, including expression of the viral products responsible for FcR induction. In all the responding HSV-infected LCL, induction of FcR always paralleled the expression of HSV antigens. Synthesis of HSV-induced FcR was shown to be inhibited by phosphonoacetic acid, an inhibitor of herpesvirus DNA polymerase activity, whereas FcR of non-HSV origin was found to be resistant to inhibitor. This would infer that HSV codes for an FcR which can be differentiated from that of cellular origin by using phosphonoacetic acid. Therefore, two different mechanisms of FcR synthesis may be suggested, one virus mediated and the second probably under cellular control. In addition, the data obtained using Epstein-Barr virus producer as well as isogeneic monoclonal cell lines, with and without the Epstein-Barr virus genome, indicated that the resident Epstein-Barr virus genome in the target cell did not have a detectable effect in the induction of FcR by HSV.