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猴细胞流产感染期间人腺病毒2型晚期转录单位mRNA的加工缺陷

Defective processing of human adenovirus 2 late transcription unit mRNAs during abortive infections in monkey cells.

作者信息

Ross D, Ziff E

机构信息

Kaplan Cancer Center, New York University Medical Center, New York 10016.

出版信息

Virology. 1994 Jul;202(1):107-15. doi: 10.1006/viro.1994.1327.

DOI:10.1006/viro.1994.1327
PMID:8009825
Abstract

Growth of human adenoviruses is severely restricted in monkey cells. We examined the synthesis of mRNAs from the Ad2 late transcription unit (LTU) in abortively infected monkey cells at late times in infection. All L2, L3, and L5 mRNAs were absent or drastically reduced in abortive infections. Most L1 and L4 mRNAs were also greatly decreased in abortive infections; however, a single large messenger was produced from each of the L1 and L4 families, at levels approaching those found in productive infections. The pattern of i-leader containing mRNAs was also changed in abortive infections. These defects could be corrected in monkey cells by the presence of SV40 T antigen or an altered adenoviral DNA binding protein. These defects in late gene expression in abortive infections could not be attributed to differences in transcription along the LTU or levels of DNA replication. In abortively infected cells, nuclear levels of L5 mRNA were decreased 2 to 6 fold, while cytoplasmic levels were decreased over 200-fold. These findings imply a general defect in processing of viral mRNAs, most likely due to defective splicing and/or transport, during abortive infections.

摘要

人类腺病毒在猴细胞中的生长受到严重限制。我们检测了在感染后期被流产感染的猴细胞中,腺病毒2型晚期转录单元(LTU)的mRNA合成情况。在流产感染中,所有L2、L3和L5 mRNA均缺失或大幅减少。大多数L1和L4 mRNA在流产感染中也大幅减少;然而,L1和L4家族各自产生了一个单一的大信使RNA,其水平接近在生产性感染中发现的水平。在流产感染中,含i-前导序列的mRNA模式也发生了变化。在猴细胞中,SV40 T抗原的存在或改变的腺病毒DNA结合蛋白可以纠正这些缺陷。流产感染中晚期基因表达的这些缺陷不能归因于沿LTU的转录差异或DNA复制水平。在流产感染的细胞中,L5 mRNA的核水平降低了2至6倍,而细胞质水平降低了200多倍。这些发现表明,在流产感染期间,病毒mRNA加工存在普遍缺陷,最有可能是由于剪接和/或转运缺陷所致。

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