Dubovi E J, Youngner J S
J Virol. 1976 May;18(2):534-41. doi: 10.1128/JVI.18.2.534-541.1976.
Purified defective interfering (DI) particles of vesicular stomatitis virus (VSV) inhibit the replication of a heterologous virus, pseudorabies virus (PSR), in hamster (BHK-21) and rabbit (RC-60) cell lines. In contrast to infectious B particles of VSV, UV irradiation of DI particles does not reduce their ability to inhibit PSR replication. However, UV irradiation progressively reduces the ability of DI particles to cause homologous interference with B particle replication. Pretreatment with interferon does not affect the ability of DI particles to inhibit PSR replication in a rabbit cell line (RC-60) in which RNA, but not DNA, viruses are sensitive to the action of interferon. Under similar conditions of interferon pretreatment, the inhibition of PSR by B particles is blocked. These data suggest that de novo VSV RNA or protein synthesis is not required for the inhibition of PSR replication by DI particles. DI particles that inhibit PSR replication also inhibit host RNA and protein synthesis in BHK-21 and RC-60 cells. Based on the results described and data in the literature, it is proposed that the same component of VSV B and DI particles is responsible for most, if not all, of the inhibitory activities of VSV, except homologous interference.
纯化的水疱性口炎病毒（VSV）缺陷干扰（DI）颗粒可抑制异源病毒伪狂犬病病毒（PSR）在仓鼠（BHK - 21）和兔（RC - 60）细胞系中的复制。与VSV的感染性B颗粒不同，DI颗粒经紫外线照射后并不降低其抑制PSR复制的能力。然而，紫外线照射会逐渐降低DI颗粒对B颗粒复制产生同源干扰的能力。在兔细胞系（RC - 60）中，用干扰素预处理并不影响DI颗粒抑制PSR复制的能力，在该细胞系中RNA病毒（而非DNA病毒）对干扰素的作用敏感。在类似的干扰素预处理条件下，B颗粒对PSR的抑制作用被阻断。这些数据表明，DI颗粒抑制PSR复制并不需要VSV的从头RNA或蛋白质合成。抑制PSR复制的DI颗粒也会抑制BHK - 21和RC - 60细胞中的宿主RNA和蛋白质合成。根据所述结果和文献数据，有人提出VSV B颗粒和DI颗粒的相同成分负责VSV的大部分（如果不是全部）抑制活性，但同源干扰除外。
