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

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Abstract
The induction of Fc receptor (FcR) in different types of lymphoid cell lines (LCL) [human and marmoset] infected with herpes simplex virus (HSV) was investigated. 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 thus possible. FcR detection was carried out by a rosette assay using ox erythrocytes coated with 7S immunoglobulin G (EA rosettes). HSV types 1 and 2 induced FcR in B [bone marrow-derived], T [thymus-derived] and null (i.e., non-B, non-T) type LCL; 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. The time course of HSV-induced FcR expression differed among these LCL types tested. Several 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 inhibited by phosphonoacetic acid, an inhibitor of herpesvirus DNA polymerase activity; FcR of non-HSV origin was resistant to inhibitor. Thus HSV codes for an FcR which can be differentiated from that of cellular origin by using phosphonoacetic acid. Two different mechanisms of FcR synthesis may exist: 1 virus mediated and the 2nd probably under cellular control. Data obtained using Epstein-Barr virus producer and 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.