Inglis S C, Brown C M
J Gen Virol. 1984 Jan;65 ( Pt 1):153-64. doi: 10.1099/0022-1317-65-1-153.
Spliced transcripts of influenza A (fowl plague) virus (FPV) RNA (vRNA) segments 7 and 8 accumulate to a much greater extent during non-productive infection of mouse L cells, than they do during productive infection in primary chick embryo fibroblasts (CEF). Virus-specific protein synthesis, or a consequent event in virus replication appears necessary to promote splicing of vRNA segment 8-encoded mRNAs in both cell types, and of vRNA segment 7-encoded mRNAs in CEF. In L cells, however, splicing of the segment 7-encoded mRNAs seems to be independent of such virus-specific control. This observation is discussed in relation to the defect in expression of vRNA 7 which has been observed previously in FPV-infected L cells, and which is thought to account for the failure of virus replication.
甲型流感(禽瘟)病毒(FPV)RNA(vRNA)片段7和8的剪接转录本,在小鼠L细胞的非生产性感染过程中积累的程度,比在原代鸡胚成纤维细胞(CEF)的生产性感染过程中积累的程度要大得多。病毒特异性蛋白质合成,或病毒复制中的后续事件,似乎是促进两种细胞类型中vRNA片段8编码的mRNA剪接以及CEF中vRNA片段7编码的mRNA剪接所必需的。然而,在L细胞中,片段7编码的mRNA的剪接似乎独立于这种病毒特异性控制。结合先前在FPV感染的L细胞中观察到的vRNA 7表达缺陷来讨论这一观察结果,该缺陷被认为是病毒复制失败的原因。