Doerig C, Beard P, Hirt B
Virology. 1987 Apr;157(2):539-42. doi: 10.1016/0042-6822(87)90297-2.
The human parvovirus B19 causes aplastic crises in sickle cell anemia patients and the disease erythema infectiosum. So far, it has not been possible to grow B19 virus in cultured cells. Here we report the use of in vitro transcription in HeLa cell extracts and transient expression of cloned DNA transfected into HeLa cells to detect and map a strong transcriptional promoter on the B19 genome. The promoter is located near the left end of the B19 genome, at position 6 map units in the clone pYT103 (approximately 280 bp upstream of the first HindIII site), and directs transcription to the right. These results suggest that the strictly limited host range of B19 does not operate at the level of transcription from the promoter at the left end of the genome.
人细小病毒B19可导致镰状细胞贫血患者发生再生障碍性危象以及引发传染性红斑。到目前为止,尚无法在培养细胞中培养B19病毒。在此我们报告利用HeLa细胞提取物中的体外转录以及转染入HeLa细胞的克隆DNA的瞬时表达来检测和定位B19基因组上一个强大的转录启动子。该启动子位于B19基因组左端附近,在克隆pYT103中位于图谱单位6处(在第一个HindIII位点上游约280 bp处),并指导转录向右进行。这些结果表明,B19严格受限的宿主范围并非在基因组左端启动子的转录水平起作用。