Shanley J D, Pesanti E L
Infect Immun. 1980 Sep;29(3):1152-9. doi: 10.1128/iai.29.3.1152-1159.1980.
Murine cytomegalovirus was found to replicate in lung and peritoneal macrophages of both CF-1 and BALB/c mice in vitro. Cytopathic changes typical of cytomegalovirus infection, including intranuclear inclusions, developed within the infected cells and eventually resulted in death of infected macrophages. Viral antigens were demonstrable by indirect immunofluorescence microscopy, and morphologically typical herpesvirus particles were observed in both nuclei and cytoplasm of murine cytomegalovirus-infected macrophages. Within 24 h after infection, at which time there was expression of viral antigens but no marcophage death, murine cytomegalovirus-infected macrophages demonstrated marked inhibition of phagocytosis of Staphylococcus aureus. Direct inhibition of macrophage function by cytomegalovirus infection in vivo could impair pulmonary defenses and may account in part for the frequent association of cytomegalovirus infection with other infectious agents.
研究发现,鼠巨细胞病毒可在体外于CF-1和BALB/c小鼠的肺巨噬细胞和腹腔巨噬细胞中复制。在受感染细胞内出现了典型的巨细胞病毒感染所致的细胞病变效应,包括核内包涵体,最终导致受感染巨噬细胞死亡。通过间接免疫荧光显微镜可检测到病毒抗原,并且在鼠巨细胞病毒感染的巨噬细胞核和细胞质中均观察到形态典型的疱疹病毒颗粒。感染后24小时内,此时虽有病毒抗原表达但巨噬细胞未死亡,鼠巨细胞病毒感染的巨噬细胞对金黄色葡萄球菌的吞噬作用受到显著抑制。体内巨细胞病毒感染对巨噬细胞功能的直接抑制可能会损害肺部防御功能,这可能部分解释了巨细胞病毒感染与其他感染因子频繁关联的原因。