zur Hausen H, Fresen K O
IARC Sci Publ (1971). 1978(20):391-6.
Infection of cells of the EBV-free human B-lymphoma lines BJAB and Ramos resulted in conversion of these cells to EBV-genome carriers expressing EBNA. EBV isolates from P3HR-1 cells induced a heterogeneous EBNA pattern: both a faintly granular pattern and brilliant EBNA-expression were observed. The two types of EBNA-expressing cells could be separated upon cloning. Brilliantly EBNA-expressing cells always segregated varying percentages of EBNA-negative cells. An EBNA-negative subclone derived from these cells was devoid of detectable EBV DNA. Nucleic acid hybridization experiments failed to reveal a correlation between the intensity of EBNA expression and the number of EBV genome equivalents per cell. EBV genome-containing cells had an average of 14-fold more cells showing EA synthesis after superinfection by P3HR-1 virus, when compared with EBNA-negative cells infected under identical conditions. Studies on the kinetics of EA induction in EBNA-positive and EBNA-negative cells indicate that complementation is required for the induction of EA after superinfection.
无EBV的人B淋巴瘤细胞系BJAB和Ramos的细胞感染导致这些细胞转化为表达EBNA的EBV基因组携带者。从P3HR - 1细胞分离出的EBV诱导出异质性的EBNA模式:观察到微弱的颗粒状模式和明亮的EBNA表达。两种类型的表达EBNA的细胞在克隆时可以分离。明亮表达EBNA的细胞总是分离出不同比例的EBNA阴性细胞。从这些细胞衍生出的一个EBNA阴性亚克隆没有可检测到的EBV DNA。核酸杂交实验未能揭示EBNA表达强度与每个细胞中EBV基因组当量数之间的相关性。与在相同条件下感染的EBNA阴性细胞相比,含EBV基因组的细胞在被P3HR - 1病毒超感染后,平均有14倍更多的细胞显示EA合成。对EBNA阳性和EBNA阴性细胞中EA诱导动力学的研究表明,超感染后诱导EA需要互补作用。