Miller D G, Miller A D
Fred Hutchinson Cancer Research Center, Seattle, Washington 98104.
J Virol. 1992 Jan;66(1):78-84. doi: 10.1128/JVI.66.1.78-84.1992.
Chinese hamster ovary (CHO) cells are resistant to infection by all of the major classes of murine retroviruses and are partially resistant to infection by gibbon ape leukemia virus. Treatment of CHO cells with the glycosylation inhibitor tunicamycin rendered these cells susceptible to infection by retroviral vectors with ecotropic, xenotropic, and amphotropic host ranges and increased the titer of gibbon ape leukemia virus pseudotyped vectors 10-fold. Vectors having a polytropic host range did not infect CHO cells in the presence or absence of tunicamycin, showing that the effect of tunicamycin was specific and related to the pseudotype of the vector. We present evidence for three mechanisms of resistance to infection: lack of viral receptors on CHO cells, the presence of nonfunctional receptors which can be made functional by treatment with tunicamycin, and the secretion of a protein factor that blocks retroviral infection of CHO cells. Several criteria indicate that the secreted inhibitor is not an interferon, and secretion of this factor was not detected in several other cell lines that were examined.
中国仓鼠卵巢（CHO）细胞对所有主要类别的鼠逆转录病毒感染具有抗性，并且对长臂猿白血病病毒感染具有部分抗性。用糖基化抑制剂衣霉素处理CHO细胞，使这些细胞易受具有亲嗜性、异嗜性和双嗜性宿主范围的逆转录病毒载体感染，并使长臂猿白血病病毒假型载体的滴度提高了10倍。无论有无衣霉素，具有多嗜性宿主范围的载体都不会感染CHO细胞，这表明衣霉素的作用是特异性的，且与载体的假型有关。我们提供了三种抗感染机制的证据：CHO细胞上缺乏病毒受体、存在可通过衣霉素处理使其具有功能的无功能受体，以及分泌一种阻断CHO细胞逆转录病毒感染的蛋白质因子。几个标准表明分泌的抑制剂不是干扰素，并且在其他几个检测的细胞系中未检测到该因子的分泌。
