Radiobiological Inactivation of Epstein-Barr Virus
- 1 January 1978
- journal article
- research article
- Published by American Society for Microbiology in Journal of Virology
- Vol. 25 (1), 51-59
- https://doi.org/10.1128/jvi.25.1.51-59.1978
Abstract
Lymphocyte tranforming properties of B95-8 strain Epstein-Barr virus (EBV) are very sensitive to inactivation by 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 2 viruses. A large part, or perhaps all, of the EBV genome is probably 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. The abilities of the virus to transform and to replicate complete progeny are probably 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 P3HR-1 strain of EBV. Based on radiobiological inactivation, 10-50% 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 [human Burkitt''s lymphoma] Raji or in P3HR-1 converted EBV genome-free cells clone B1. The resident EBV genome apparently participates in the early antigen induction process. Variation in radiobiological killing of B95-8 and P3HR-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.This publication has 34 references indexed in Scilit:
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