Lvovsky E, Levine P H, Fuccillo D, Ablashi D V, Bengali Z H, Armstrong G R, Levy H B
J Natl Cancer Inst. 1981 Jun;66(6):1013-9. doi: 10.1093/jnci/66.6.1013.
The in vitro sensitivity of oncogenic herpesviruses, Epstein-Barr virus (EBV), and Herpesvirus saimiri (HVS) to human interferon produced by normal human leukocytes (Le), lymphoblastoid cell lines (LYI), and diploid fibroblasts (Fi) was studied. Four virus strains were used: HVS S295C, the highly oncogenic HVS S396-O, the transforming B95-8 strain of EBV, and the nontransforming P3HR1 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(I).poly(C) and the complex of poly(I).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(I).poly(C). In Raji cells superinfected with P3HR1-EBV, polynucleotides failed to stimulate interferon, and higher EBV-induced EA expression was observed. The percentage of P3HR1 and Raji cells spontaneously expressing EBV-associated antigens remained unchanged after exposure to either interferon or polynucleotides.
研究了致癌性疱疹病毒、爱泼斯坦-巴尔病毒（EBV）和赛米利疱疹病毒（HVS）对正常人白细胞（Le）、淋巴母细胞系（LYI）和二倍体成纤维细胞（Fi）产生的人干扰素的体外敏感性。使用了四种病毒株：HVS S295C、高致癌性的HVS S396 - O、EBV的转化株B95 - 8以及EBV的非转化株P3HR1。当将HVS和P3HR1 - EBV吸附到细胞上后再应用所有干扰素时，它们均具有活性，尽管达到50%抑制HVS诱导的细胞病变效应或EBV诱导的早期抗原（EA）表达所需的干扰素量不同。只有Le和LYI能阻止EBV的B95 - 8株对人脐带血淋巴细胞（HCBL）的转化。在这些实验中，致癌性疱疹病毒最有效的抑制剂是Le，最无效的是Fi。还研究了多核苷酸聚（I）·聚（C）以及聚（I）·聚（C）与聚-L-赖氨酸和羧甲基纤维素的复合物对HVS和EBV的作用。它们的抑制作用与疱疹病毒感染细胞产生干扰素的能力成比例。因此，产生相对高水平干扰素的猫头鹰猴肾细胞只需纳克量的多核苷酸就能对HVS产生抗性。聚（I）·聚（C）也能阻止B95 - 8 - EBV对HCBL的转化。在被P3HR1 - EBV超感染的Raji细胞中，多核苷酸未能刺激干扰素产生，且观察到更高的EBV诱导的EA表达。暴露于干扰素或多核苷酸后，自发表达EBV相关抗原的P3HR1和Raji细胞的百分比保持不变。
