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爱泼斯坦-巴尔病毒的放射生物学失活

Radiobiological inactivation of Epstein-Barr virus.

作者信息

Henderson E, Heston L, Grogan E, Miller G

出版信息

J Virol. 1978 Jan;25(1):51-9. doi: 10.1128/JVI.25.1.51-59.1978.

Abstract

Lymphocyte transforming properties of B95-8 strain Epstein-Barr virus (EBV) are very sensitive to inactivation by either UV or X irradiation. No dose of irradiation increases the transforming capacity of EBV. The X-ray dose needed for inactivation of EBV transformation (dose that results in 37% survival, 60,000 rads) is similar to the dose required for inactivation of plaque formation by herpes simplex virus type 1 (Fischer strain). Although herpes simplex virus is more sensitive than EBV to UV irradiation, this difference is most likely due to differences in the kinetics or mechanisms of repair of UV damage to the two viruses. The results lead to the hypothesis that a large part, or perhaps all, of the EBV genome is in some way needed to initiate transformation. The abilities of EBV to stimulate host cell DNA synthesis, to induce nuclear antigen, and to immortalize are inactivated in parallel. All clones of marmoset cells transformed by irradiated virus produce extracellular transforming virus. These findings suggest that the abilities of the virus to transform and to replicate complete progeny are inactivated together. The amounts of UV and X irradiation that inactivate transformation by B95-8 virus are less than the dose needed to inactivate early antigen induction by the nontransforming P(3)HR-1 strain of EBV. Based on radiobiological inactivation, 10 to 50% of the genome is needed for early antigen induction. Inactivation of early antigen induction is influenced by the cells in which the assay is performed. Inactivation proceeds more rapidly in EBV genome-free cells than in genome carrier Raji or in P(3)HR-1 converted EBV genome-free cells clone B(1). These results indicate that the resident EBV genome participates in the early antigen induction process. Variation in radio-biological killing of B95-8 and P(3)HR-1 EBV is not attributable to variations in the repair capacities of the cells in which the viruses were assayed, since inactivation of HSV was the same in primary lymphocytes and in all lymphoid cell lines tested.

摘要

B95-8株爱泼斯坦-巴尔病毒(EBV)的淋巴细胞转化特性对紫外线或X射线照射的灭活非常敏感。任何剂量的照射都不会增加EBV的转化能力。使EBV转化失活所需的X射线剂量(导致37%存活的剂量,60000拉德)与使1型单纯疱疹病毒(费舍尔株)蚀斑形成失活所需的剂量相似。虽然单纯疱疹病毒比EBV对紫外线照射更敏感,但这种差异很可能是由于两种病毒紫外线损伤修复的动力学或机制不同。这些结果引出一个假说,即EBV基因组的很大一部分,或者也许是全部,在某种程度上是启动转化所必需的。EBV刺激宿主细胞DNA合成、诱导核抗原和使细胞永生化的能力同时失活。经照射病毒转化的狨猴细胞的所有克隆都产生细胞外转化病毒。这些发现表明,病毒转化和复制完整子代的能力同时失活。使B95-8病毒转化失活的紫外线和X射线照射量小于使非转化性EBV的P(3)HR-1株诱导早期抗原失活所需的剂量。根据放射生物学灭活,诱导早期抗原需要10%至50%的基因组。早期抗原诱导的失活受进行检测的细胞影响。在无EBV基因组的细胞中,失活比在基因组载体Raji细胞或P(3)HR-1转化的无EBV基因组细胞克隆B(1)中进行得更快。这些结果表明,常驻的EBV基因组参与早期抗原诱导过程。B95-8和P(3)HR-1 EBV放射生物学杀伤的差异不归因于检测病毒的细胞修复能力的差异,因为单纯疱疹病毒在原代淋巴细胞和所有测试的淋巴细胞系中的失活情况相同。

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