人肿瘤细胞株中细小病毒H—1的DNA扩增与非结构蛋白NS—1基因的表达

DNA amplification and non-structural protein NS-1 gene expression of parvovirus H-1 in human cancer cell lines

研究三株人癌细胞和两株对照细胞对细小病毒Ｈ－１杀伤作用敏感性的分子机制．表明了在感染复数ｍｏｉ（ｍｕｌｔｉｐｉｃｉｔｙｏｆｉｎｆｅｃｔｉｏｎ）为５ｐｆｕ（ｐｌａｑｕｅｆｏｒｍｉｎｇｕｎｉｔ）／细胞的情况下，作为Ｈ—１病毒复制受纳细胞的人肝癌细胞株ＯＧＹ－７７０３和人胃癌细胞株ＳＧＣ—７９０１，能够支持病毒ＤＮＡ扩增和非结构蛋白ＮＳ—１基因的表达，这和作为阳性对照的由ＳＶ４０转化的新生儿肾细胞株ＮＢ—Ｋ一样，但对Ｈ—１病毒感染有抗性的人肾癌细胞株ＯＵＲ—１０和它的对照人胎肾细胞株ＨｕＫ—１，并不支持病毒ＤＮＡ扩增和ＮＳ—１蛋白的表达．本文结果指出，细小病毒Ｈ—１的杀伤作用与细胞中的病毒ＤＮＡ扩增及ＮＳ—１基因表达的程度相关．

The molecular m echanism of sensitization to killing by parvovirus H-1 in three human cancer cell lines and two control cell lines was studied. It was shown that with a multiplicity of infection(m. o. i.)of 5 plaque-forming units(p. f. u.) per cell, the human hepatoma cell line QGY-7703 and the gastric carcinoma cell line SGC-7901, both known to be permissive to H-1 rep licati on, could support viral DNA amplification and viral non-structural protein NS-1 gene expression.The same was true for the cell line NB-K, a new-born human kidney cell line transformed by SV 40; but not so for the human renal carcinoma cell line OUR-10 and its counterpart HuK-1, a human fetal kidney cell line, the latter two were resistant to H-1 infection. The results indicated that the killing effect of parvovirus H-1 was related to the degree of DNA replication and NS-1 gene expression.