O'Sullivan M A, Killen H M
Department of Microbiology, Moyne Institute, Trinity College, University of Dublin, Ireland.
J Gen Virol. 1994 Sep;75 ( Pt 9):2387-92. doi: 10.1099/0022-1317-75-9-2387.
This study describes the susceptibility to dengue virus infection of a monocytic cell line at different states of differentiation. Infectious virus titres increased in undifferentiated U937 cells following infection with clinical isolates but only when the cells were infected via their Fc receptors. No. c.p.e. was observed and virus was not secreted into supernatant fluid. Once differentiated, cells were susceptible to infection either with virus alone or with virus-antibody complexes. Infection was cytolytic and virus was released into the supernatant fluid. Similar results were obtained with freshly isolated peripheral blood monocytes. Increased blood vessel permeability, which occurs in dengue haemorrhagic fever and dengue shock syndrome patients, has been correlated with secondary heterotypic infections and has been postulated to arise from antibody-enhanced infection of monocytes. The data presented suggest a possible mechanism whereby infected monocytes undergoing diapedesis through blood vessel walls might differentiate sufficiently during the process to release virus and cytokines at localized sites on blood vessels.
本研究描述了处于不同分化状态的单核细胞系对登革病毒感染的易感性。临床分离株感染未分化的U937细胞后,感染性病毒滴度升高,但仅当细胞通过其Fc受体被感染时才会出现这种情况。未观察到细胞病变效应,且病毒未分泌到上清液中。一旦分化,细胞对单独的病毒或病毒 - 抗体复合物感染均敏感。感染具有细胞溶解性,病毒被释放到上清液中。新鲜分离的外周血单核细胞也获得了类似结果。登革出血热和登革休克综合征患者出现的血管通透性增加与继发性异型感染相关,并推测是由单核细胞抗体增强感染引起的。所呈现的数据表明了一种可能的机制,即通过血管壁进行渗出的受感染单核细胞在这个过程中可能充分分化,从而在血管局部部位释放病毒和细胞因子。