仙台病毒（副流感病毒I型）对多瘤病毒合成的短暂抑制作用。II. 灭活病毒的干扰机制。
Transient inhibition of polyoma virus synthesis by sendai virus (parainfluenza I). II. Mechanism of the interference by inactivated virus.
作者信息
Smith G L, Consigli R A
出版信息
J Virol. 1972 Dec;10(6):1098-108. doi: 10.1128/JVI.10.6.1098-1108.1972.
The mechanism of the transient inhibition of polyoma virus synthesis by betapropiolactone-inactivated Sendai virus was studied. Polyoma virus early functions did not appear to be affected, although deoxyribonucleic acid (DNA) and structural protein synthesis were inhibited 60 and 35% respectively. The inhibition of macromolecular synthesis was not sufficient to account for the 90% inhibition of infectious progeny formation. Encapsidation of polyoma DNA into mature virions appears to be completely inhibited after superinfection by beta-propiolactone-inactivated Sendai virus. Ultraviolet irradiation of live or beta-propiolactone-inactivated Sendai virus preparations abolishes the interfering capacity, indicating that a functional Sendai virus ribonucleic acid molecule is the interfering component.
研究了β-丙内酯灭活的仙台病毒对多瘤病毒合成的瞬时抑制机制。多瘤病毒的早期功能似乎未受影响，尽管脱氧核糖核酸（DNA）和结构蛋白合成分别被抑制了60%和35%。大分子合成的抑制不足以解释感染性子代形成90%的抑制率。在被β-丙内酯灭活的仙台病毒超感染后，多瘤病毒DNA包装到成熟病毒粒子中的过程似乎被完全抑制。对活的或β-丙内酯灭活的仙台病毒制剂进行紫外线照射可消除干扰能力，这表明功能性仙台病毒核糖核酸分子是干扰成分。
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