Mills J
Am Rev Respir Dis. 1979 Dec;120(6):1239-44. doi: 10.1164/arrd.1979.120.6.1239.
Cultured mouse alveolar macrophages supported the growth of Sendai virus (murine parainfluenza I virus), as measured by both a 10-fold increase in extracellular virus titers and development of viral antigens on most of the cells. Synthesis of virus continued for at least 1 month without cytopathic effects. Macrophage phagocytic activity for Candida, Staphylococcus epidermidis, and opsonized erythrocytes remained unaffected by the infection, and the ability of the cells to kill S. epidermidis and S. Aureus was also unchanged. The defects in alveolar macrophage function observed in Sendai-infected mouse lungs probably are not due to a direct effect of the virus on macrophage function.
通过细胞外病毒滴度增加10倍以及大多数细胞上病毒抗原的出现来衡量,培养的小鼠肺泡巨噬细胞支持仙台病毒(鼠副流感I病毒)的生长。病毒合成持续至少1个月而无细胞病变效应。巨噬细胞对念珠菌、表皮葡萄球菌和调理红细胞的吞噬活性不受感染影响,细胞杀灭表皮葡萄球菌和金黄色葡萄球菌的能力也未改变。在感染仙台病毒的小鼠肺中观察到的肺泡巨噬细胞功能缺陷可能并非病毒对巨噬细胞功能的直接影响所致。