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辅助细胞对缺陷型F病毒回收的特异性。

Helper specificity for retrieval of defective friend virus.

作者信息

Fieldsteel A H, Kurahara C, Dawson P J

出版信息

Int J Cancer. 1975 Mar 15;15(3):522-7. doi: 10.1002/ijc.2910150318.

Abstract

A Friend virus-induced reticulum-cell sarcoma from BALB/c mice has been cultivated in vitro in our laboratory for more than 11 years and contains no detectable evidence of virus. However, Friend virus could be retrieved readily from the tissue cultures by any of several lymphatic leukemia viruses belonging to the Friend-Moloney-Rauscher (FMR) group, as long as the helper viruses were actively replicating in a culture. Helper activity appeared to be highly specific and limited to the FMR group including the B-tropic Tennant leukemia virus which produced a B-tropic Friend virus pseudotype. The naturally occurring type AKR murine leukemia viruses and the related Gross passage A virus failed both in vivo and in vitro to retrieve the Friend virus genome from the virus-free tumor cells.

摘要

我们实验室已在体外培养源自BALB/c小鼠的一种友病毒诱导的网状细胞肉瘤超过11年,且未检测到病毒迹象。然而,只要辅助病毒在培养物中活跃复制,通过属于Friend-Moloney-Rauscher(FMR)组的几种淋巴白血病病毒中的任何一种,都能轻易从组织培养物中找回友病毒。辅助活性似乎具有高度特异性,仅限于FMR组,包括产生B嗜性友病毒假型的B嗜性坦南特白血病病毒。天然存在的AKR型鼠白血病病毒及相关的格罗斯传代A病毒在体内和体外均未能从无病毒的肿瘤细胞中找回友病毒基因组。

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