Epstein-Barr Virus and Herpesvirus saimiri: Sensitivity to Interferons and Interferon Inducers2

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Abstract
The In vitro sensitivity of oncogenic herpesvlruses, Epstein-Barr virus (EBV), and Herpesvirus saimiri (HVS) to human interferon produced by normal human leukocytes (le), Iymphoblastoid cell lines (LYI), and diploid fibroblasts (Fi) was studied. Four virus strains were used: HVS S295C, the highly oncogenic HVS 8396-0, the transforming B95-8 strain of EBV, and the nontransforming P3HRl strain of EBV. All interferons were active when applied to the cells after absorption of HVS and P3HR1-EBV, although different amounts were required to achieve 50% inhibition of HVS-induced cytopathic effect or EBV-induced early antigen (EA) expression. Transformation of human umbilical cord blood lymphocytes (HCBl) by the B95-8 strain of EBV was prevented only by Le and LYI. In these experiments, the most effective inhibitor of the oncogenic herpesviruses was Le, and the least effective was Fi. The effect of polynucleotides poly(l)-poly(C) and the complex of poly(l)-poly(C) with poly-L-lysine and carboxymethylcellulose on HVS and EBV was also studied. Their inhibitory action was proportionate to the ability of herpesvirus-infected cells to produce interferon. Thus owl monkey kidney cells, which produce relatively high levels of interferon, required nanogram quantities of polynucleotides to become resistant to HVS. Transformation of HCBl by B95-8-EBV was also prevented by poly(l)-poly(C). In Raji cells superinfected with P3HR1-EBV, polynucleotldes failed to stimulate interferon, and higher EBV-induced EA expression was observed. The percentage of P3HRl and Raji cells spontaneously expressing EBV-associated antigens remained unchanged after exposure to either interferon or polynucleotides.