Balduzzi P C
J Virol. 1967 Jun;1(3):509-13. doi: 10.1128/JVI.1.3.509-513.1967.
Ultraviolet light (UV) impaired the capacity of L cells to support growth of encephalomyocarditis virus. The loss of capacity was partially restored by high multiplicity of infection (MOI). This phenomenon was not due to an increased probability of an infectious virus particle reaching a site of replication undamaged by UV, since UV-inactivated virus at high MOI induced restoration of the capacity to support multiplication of nonirradiated virus adsorbed at low MOI. Multiplicity reactivation of UV-irradiated virus did not play a role in this phenomenon since restoration of capacity took place without multiplication of the UV-irradiated restoring virus. The evidence indicates that restoration of capacity was not due to viral interactions involving genetic exchange. The ability to restore capacity was a property more radioresistant than infectivity, suggesting that the former is a function only of part of the viral genome.
紫外线（UV）损害了L细胞支持脑心肌炎病毒生长的能力。通过高感染复数（MOI）可部分恢复这种能力丧失。这种现象并非由于感染性病毒颗粒到达未被UV损伤的复制位点的概率增加，因为高MOI的UV灭活病毒可诱导恢复支持低MOI吸附的未照射病毒增殖的能力。UV照射病毒的多重复活在这一现象中不起作用，因为能力的恢复在未照射恢复病毒增殖的情况下发生。证据表明，能力的恢复并非由于涉及基因交换的病毒相互作用。恢复能力的特性比感染性更具放射抗性，这表明前者仅是病毒基因组一部分的功能。
