Type C retrovirus inactivation by human complement is determined by both the viral genome and the producer cell
Type C retrovirus inactivation by human complement is determined by both the viral genome and the producer cell
复制标题
人类补体对 C 型逆转录病毒的灭活由病毒基因组和生产细胞共同决定
作者：
Y. Takeuchi;F. Cosset;P. Lachmann;H. Okada;R. Weiss;M. Collins
人血清对C型逆转录病毒的灭活可能是体内使用逆转录病毒载体进行基因治疗的一个相当大的障碍。在这里，我们表明，病毒灭活是依赖于病毒和用于生产病毒的细胞系。从鼠NIH 3 T3或狗Cf2 ThS +L-细胞产生的所有病毒对人血清敏感。相比之下，从貂Mv-1-Lu和人HOS或TE 671细胞产生的那些病毒至少部分具有抗性，但鼠白血病病毒除外。特别地，当从Mv-1-Lu或HOS细胞产生时，猫内源性病毒RD 114对一组8种人血清完全具有抗性。这种差异性抗性由病毒包膜蛋白控制。病毒灭活可与生产细胞被人血清裂解的能力相关。敏感病毒的灭活需要经典的补体途径，但不需要病毒体裂解。
The inactivation of type C retroviruses by human serum may be a considerable impediment to the use of retroviral vectors in vivo for gene therapy. Here we show that virus inactivation is dependent both on the virus and on the cell line used to produce the virus. All viruses produced from murine NIH 3T3 or dog Cf2ThS+L- cells are sensitive to human serum. In contrast, those produced from mink Mv-1-Lu and human HOS or TE671 cells are at least partially resistant, with the exception of murine leukemia viruses. In particular, the feline endogenous virus RD114 is completely resistant to a panel of eight human sera when produced from Mv-1-Lu or HOS cells. This differential resistance is controlled by the viral envelope proteins. Virus inactivation can be correlated with the ability of the producer cells to be lysed by human serum. Inactivation of sensitive viruses requires the classical pathway of complement but does not require virion lysis.
影响因子：
3.7
作者：
MARKOWITZ, D;GOFF, S;BANK, A
通讯作者：
BANK, A
辛德比斯病毒唾液酸含量的宿主修饰影响替代补体途径激活和病毒清除。
DOI：
--
发表时间：
1981
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Hirsch,RL;Griffin,DE;Winkelstein,JA
通讯作者：
Winkelstein,JA