Natuk R J, Holowczak J A
Virology. 1985 Dec;147(2):354-72. doi: 10.1016/0042-6822(85)90138-2.
Primary macrophage cultures were prepared from the peritoneal exudate cell population harvested from mice challenged intraperitoneally with saline, thioglycollate, or vaccinia virus. Vaccinia virus was adsorbed and penetrated into primary macrophages and L-cells with similar kinetics. As evidenced by the expression of some "early" virus-specified proteins, partial uncoating and activation of the virion-associated DNA-dependent RNA polymerase occurred in the infected macrophages. Subsequently, the viral replication cycle in macrophages was aborted; with time after infection, viral DNA and virion proteins initially associated with infected cells could be detected in an acid-soluble form in the medium harvested from infected macrophage cultures. The results suggest that at the time that the final stages of virus uncoating should have occurred, intracellular subviral particles were, instead, degraded in the infected, primary macrophages. Viral DNA synthesis could not be measured in vaccinia virus-infected macrophages, no "late" virus functions were expressed, and progeny virions were not assembled. As measured by the binding of antiviral-antibody-125I-protein A complexes to the surface of vaccinia virus-infected cells, the expression of virus-specified antigens on the surfaces of infected macrophages was significantly reduced and never exceeded that measured at 2 hr after infection on the surfaces of infected L-cells. The expression of virus-specified polypeptides with mol mass of 48-50, 45-46, 36-37, and 25 kDa on the plasma membranes of vaccinia virus-infected, thioglycollate-elicited macrophages, rendered the infected macrophages susceptible to lysis by vaccinia virus-specific cytotoxic T-cells.
原代巨噬细胞培养物是从小鼠腹腔渗出细胞群体中制备的,这些小鼠通过腹腔注射生理盐水、巯基乙酸盐或痘苗病毒进行攻击。痘苗病毒以相似的动力学吸附并穿透原代巨噬细胞和L细胞。一些“早期”病毒特异性蛋白的表达证明,在受感染的巨噬细胞中发生了部分脱壳以及病毒粒子相关的依赖DNA的RNA聚合酶的激活。随后,巨噬细胞中的病毒复制周期中止;随着感染后时间的推移,最初与受感染细胞相关的病毒DNA和病毒粒子蛋白可以在从受感染巨噬细胞培养物中收获的培养基中以酸溶性形式被检测到。结果表明,在病毒脱壳的最后阶段应该发生的时候,细胞内亚病毒颗粒反而在受感染的原代巨噬细胞中被降解。在痘苗病毒感染的巨噬细胞中无法检测到病毒DNA合成,没有“晚期”病毒功能被表达,并且子代病毒粒子没有组装。通过抗病毒抗体-125I-蛋白A复合物与痘苗病毒感染细胞表面的结合来测量,受感染巨噬细胞表面病毒特异性抗原的表达显著降低,并且从未超过在感染后2小时在受感染L细胞表面测量到的水平。在痘苗病毒感染的、巯基乙酸盐诱导的巨噬细胞质膜上,分子量为48 - 50、45 - 46、36 - 37和25 kDa的病毒特异性多肽的表达,使受感染的巨噬细胞易被痘苗病毒特异性细胞毒性T细胞裂解。