Studies on the Induction of IgG-Fc Receptors and Synthesis of IgM in Primary and Chronically-Infected Lymphoid (Raji) Cells by Herpes Simplex Virus

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Abstract
Summary The present paper reports on the induction of two cell surface markers on human lymphoid cells following herpes simplex virus (HSV) infection. While both primary and chronic infections of human lymphoid cells led to the induction of receptors for the Fc region of 7S IgG, chronic HSV infection was also characterized by the induction of surface-bound IgM. Surface and intracellular Fc receptors were detected in the human lymphoid cell line, Raji, infected with HSV types 1 and 2. Under optimal conditions with a multiplicity of infection (m.o.i.) of 50 to 100 p.f.u. per cell, this marker was inducible in only about 53% of the infected cells. Kinetic studies revealed the appearance of these receptors at around 5 h following HSV infection and they reached a plateau 16 to 18 h p.i. Interestingly, this Fc receptor expression (i.e. percentage of positive cells) was found to be similar in primary and chronically HSV-infected Raji cells. Both human leukocyte interferon and phosphonoacetic acid (PAA), an inhibitor of herpesvirus DNA polymerase activity, effectively inhibited Fc receptor synthesis during primary HSV-infection and these two agents suppressed its induction in chronically HSV-infected Raji (Raji-HSV) cells. This inhibitory or suppressive effect, particularly of PAA, suggests that this HSV-induced Fc receptor may represent a late virus function in the infected cell. Unlike primary HSV infection, about 80% of the chronically HSV-infected Raji cells were found to express surface-bound IgM. This IgM induction was suppressed by long-term interferon treatment but not with PAA-treatment. Superinfection studies of interferon and PAA-treated Raji-HSV cells indicated that only the former would develop Fc receptors suggesting a protective role of this IgM against superinfection by HSV.