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化学致癌物4-硝基喹啉1-氧化物对人巨细胞病毒的灭活作用。

Inactivation of human cytomegalovirus by the chemical carcinogen 4-nitroquinoline 1-oxide.

作者信息

Albrecht T, Speelman D J, Li J L

出版信息

J Gen Virol. 1979 Oct;45(1):231-6. doi: 10.1099/0022-1317-45-1-231.

Abstract

The infectivity of cytomegalovirus (CMV), strain Davis, was inactivated by 4-nitroquinoline 1-oxide (NQO). A series of survival curves indicates that the rate of inactivation was directly dependent on the concentration of NQO over a range of 5 to 200 microgram/ml. At concentrations of I microgram/ml or less, inactivation of virus stock was not observed and at concentrations in excess of 200 microgram/ml, the cellular toxicity of residual NQO prevented quantification of the relatively low surviving infectivity. At a concentration of 200 microgram/ml NQO or less, the loss of virus infectivity could be clearly shown to result from the interaction of NQO with virus and not with cells, since the addition of similar doses of NQO to assay cells simultaneously with virus did not adversely affect the sensitivity of the assay cells to measure virus infectivity. Similarly, the dimethylsulphoxide carrier at concentrations of 5% or less was shown to have a negligible effect on both virus infectivity and on the sensitivity of human skin muscle cells to assay virus infectivity. NQO inactivation of virus infectivity appeared to depend very little on white light, since the kinetics of inactivation in the presence and in the absence of white light were similar.

摘要

巨细胞病毒(CMV)戴维斯株的感染性被4-硝基喹啉-1-氧化物(NQO)灭活。一系列存活曲线表明,在5至200微克/毫升的浓度范围内,灭活速率直接取决于NQO的浓度。在1微克/毫升或更低的浓度下,未观察到病毒原液的灭活,而在超过200微克/毫升的浓度下,残留NQO的细胞毒性妨碍了对相对较低存活感染性的定量。在200微克/毫升或更低的NQO浓度下,病毒感染性的丧失可明确显示是由于NQO与病毒而非细胞的相互作用所致,因为在将类似剂量的NQO与病毒同时添加到测定细胞时,并未对测定细胞测量病毒感染性的敏感性产生不利影响。同样,浓度为5%或更低的二甲基亚砜载体对病毒感染性以及人皮肤肌肉细胞测定病毒感染性的敏感性的影响可忽略不计。NQO对病毒感染性的灭活似乎很少依赖于白光,因为在有和没有白光的情况下,灭活动力学相似。

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