Ozawa K, Ayub J, Kajigaya S, Shimada T, Young N
Cell Biology Section, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892.
J Virol. 1988 Aug;62(8):2884-9. doi: 10.1128/JVI.62.8.2884-2889.1988.
The B19 parvovirus is a cause of bone marrow failure in humans. B19 is toxic to erythroid progenitor cells in vitro. Viral products possibly responsible for toxicity were explored by transfection of cloned B19 genome into HeLa cells. The nonstructural (NS) protein was detected in cells 30 h after transfection. Plasmids containing the B19 genome were transfected with selectable marker genes in stable transformation assays. Plasmids that contained the left side of the B19 genome, which encodes the NS protein of the virus, inhibited antibiotic-resistant colony formation. Transformation occurred when NS protein expression was blocked by mutation. Suppression of transformation by NS protein was not tissue specific, suggesting a role for NS protein in toxicity for nonpermissive cells without parvovirus replication or virion accumulation.
B19细小病毒是人类骨髓衰竭的一个病因。B19在体外对红系祖细胞有毒性。通过将克隆的B19基因组转染到HeLa细胞中，探索了可能导致毒性的病毒产物。转染后30小时在细胞中检测到非结构（NS）蛋白。在稳定转化试验中，将含有B19基因组的质粒与选择标记基因一起转染。含有B19基因组左侧（编码病毒NS蛋白）的质粒抑制了抗生素抗性菌落的形成。当NS蛋白表达因突变而被阻断时发生了转化。NS蛋白对转化的抑制作用不是组织特异性的，这表明NS蛋白在对没有细小病毒复制或病毒粒子积累的非允许细胞的毒性中起作用。
