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脾坏死病毒,一种禽逆转录病毒,可感染灵长类细胞。

Spleen necrosis virus, an avian retrovirus, can infect primate cells.

作者信息

Koo H M, Brown A M, Ron Y, Dougherty J P

机构信息

Department of Molecular Genetics and Microbiology, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey Rutgers, Piscataway 08854-5635.

出版信息

J Virol. 1991 Sep;65(9):4769-76. doi: 10.1128/JVI.65.9.4769-4776.1991.

Abstract

Spleen necrosis virus (SNV) is an avian retrovirus that can infect some mammalian cells such as dog cells as well as all avian cells tested to date. We were interested in testing whether SNV could also infect primate cells. For these experiments, we used HeLa and COS-7 cells. Initially, we determined whether the SNV long terminal repeat promoter was functional in HeLa and COS-7 cells. In transient transfection assays, the SNV promoter efficiently directed chloramphenicol acetyltransferase gene expression in both HeLa and COS-7 cells. Using SNV- and murine leukemia virus-derived retroviral vectors containing the neomycin phosphotransferase gene, we found that SNV established a provirus in HeLa and COS-7 cells as efficiently as did an amphotropic murine leukemia virus, as judged by the number of G418-resistant HeLa and COS-7 cell colonies obtained after infection and selection. Although SNV formed a provirus in both HeLa and COS-7 cells, productive infection of these cells was not obtained with use of replication-competent SNV. These results suggest that SNV can infect, form a provirus, and stably express a transduced gene in primate cells, but there is a posttranscriptional block to its replication in these cells.

摘要

脾坏死病毒(SNV)是一种禽逆转录病毒,它能够感染某些哺乳动物细胞,如犬类细胞,以及迄今为止测试过的所有禽类细胞。我们感兴趣的是测试SNV是否也能感染灵长类细胞。在这些实验中,我们使用了HeLa细胞和COS-7细胞。最初,我们确定SNV长末端重复启动子在HeLa细胞和COS-7细胞中是否具有功能。在瞬时转染试验中,SNV启动子在HeLa细胞和COS-7细胞中均能有效地指导氯霉素乙酰转移酶基因的表达。使用含有新霉素磷酸转移酶基因的源自SNV和鼠白血病病毒的逆转录病毒载体,我们发现,根据感染和筛选后获得的对G418耐药的HeLa细胞和COS-7细胞集落数量判断,SNV在HeLa细胞和COS-7细胞中建立前病毒的效率与双嗜性鼠白血病病毒一样高。尽管SNV在HeLa细胞和COS-7细胞中均形成了前病毒,但使用具有复制能力的SNV未能实现对这些细胞的有效感染。这些结果表明,SNV能够在灵长类细胞中感染、形成前病毒并稳定表达转导基因,但在这些细胞中其复制存在转录后障碍。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aba4/248934/d7fa4ee43788/jvirol00052-0235-a.jpg

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