Moore D L, Mills E L
Blood. 1987 Aug;70(2):351-5.
The mechanism by which influenza virus interferes with polymorphonuclear leukocyte (PMN) chemotaxis was investigated. Incubation of human PMN with influenza A virus in vitro for 30 minutes significantly decreased PMN migration under agarose in response to N-formyl-methionyl-leucyl-phenylalanine (FMLP) or zymosan-activated serum. Virus-treated PMN tended to aggregate in the under-agarose assay. Aggregation was avoided by using a more dilute PMN suspension in filter assays. Virus treatment significantly decreased migration through 100-micron thick cellulose nitrate filters but had no effect on migration through 10-micron thick polycarbonate filters or on PMN bipolar shape change. Virus was not chemotactic in the polycarbonate filter assay and did not induce shape change in purified PMN. It was concluded that influenza virus did not interfere with the ability of PMN to recognize a chemoattractant, undergo shape change, and move a short distance but did limit the extent of migration. Inhibition could not be explained by chemotactic deactivation, since the virus was not chemotactic.
研究了流感病毒干扰多形核白细胞（PMN）趋化作用的机制。将人PMN与甲型流感病毒在体外孵育30分钟，可显著降低PMN在琼脂糖下对N-甲酰甲硫氨酰亮氨酰苯丙氨酸（FMLP）或酵母聚糖激活血清的迁移。在琼脂糖下试验中，经病毒处理的PMN倾向于聚集。在滤膜试验中，使用更稀的PMN悬液可避免聚集。病毒处理显著降低了PMN通过100微米厚硝酸纤维素滤膜的迁移，但对通过10微米厚聚碳酸酯滤膜的迁移或PMN双极形态变化没有影响。在聚碳酸酯滤膜试验中，病毒没有趋化性，也不会诱导纯化的PMN发生形态变化。得出的结论是，流感病毒不会干扰PMN识别趋化因子、发生形态变化以及短距离移动的能力，但会限制迁移的程度。由于病毒没有趋化性，因此抑制作用无法用趋化失活来解释。
