Repik P, Flamand A, Bishop D H
J Virol. 1976 Oct;20(1):157-69. doi: 10.1128/JVI.20.1.157-169.1976.
The ability of certain vesicular stomatitis virus (VSV; Indiana serotype) temperature-sensitive (ts) mutants to synthesize intracellular viral complementary RNA (vcRNA) at permissive or nonpermissive temperatures for productive infections has been investigated. Mutants belonging to complementation groups II, III, and V synthesize RNA at nonpermissive temperature in amounts essentially equivalent to that obtained at permissive temperatures. Mutant ts G I-114 possesses a thermolabile transcriptase and does not synthesize vcRNA at 40 degrees C; however, mutants ts O I-5, O I-53, O I-78, and O I-80 possess thermostabile transcriptases that are capable of some vcRNA synthesis at 40 degrees C. All five group I mutants are defective in their secondary transcription ability at 40 degrees C. Wild-type VSV New Jersey virus is able to complement the transcription defect of ts G I-114 at 40 degrees C. This complementation is inhibited by puromycin, suggesting that a viral gene product of VSV New Jersey (e.g., its transcriptase or a transcriptase component) is involved. Mokola virus is not able to complement the ts G I-114 defect, although Mokola does synthesize vcRNA in infected cells (in the presence or absence of cycloheximide).
研究了某些水泡性口炎病毒(VSV;印第安纳血清型)温度敏感(ts)突变体在允许或不允许产生有感染性病毒的温度下合成细胞内病毒互补RNA(vcRNA)的能力。属于互补群II、III和V的突变体在非允许温度下合成RNA的量基本上与在允许温度下获得的量相当。突变体ts G I-114具有热不稳定的转录酶,在40℃时不合成vcRNA;然而,突变体ts O I-5、O I-53、O I-78和O I-80具有热稳定的转录酶,能够在40℃时进行一些vcRNA合成。所有五个I组突变体在40℃时的二次转录能力均有缺陷。野生型VSV新泽西病毒能够在40℃时弥补ts G I-114的转录缺陷。这种互补作用受到嘌呤霉素的抑制,表明VSV新泽西病毒的一种病毒基因产物(例如其转录酶或转录酶组分)参与其中。莫科拉病毒不能弥补ts G I-114的缺陷,尽管莫科拉病毒在感染细胞中(无论有无放线菌酮)确实能合成vcRNA。