Srivastava S, Khanna N, Saxena S K, Singh A, Mathur A, Dhole T N
Postgraduate Department of Microbiology, King George's Medical College, Lucknow, India.
Int J Exp Pathol. 1999 Feb;80(1):17-24. doi: 10.1046/j.1365-2613.1999.00092.x.
The ability of neutrophils to degrade the phagocytosed Japanese encephalitis (JE) virion, via triggering of the respiratory burst and generation of toxic radicals has been investigated. JEV or JEV-induced macrophage derived factor (MDF) induces increase in intracellular oxidative signals with generation of superoxide anion (O2-), via activation of cytosolic NADPH and subsequent formation of hydrogen peroxide, with maximum activity on day 7 post infection. The response was sensitive to anti-MDF antibody treatment. Further, the study revealed rapid degradation of phagocytosed JE viral protein and nucleic acid. The viral protein degradation was partially dependent on the generation of toxic oxygen species as it could be abrogated by pretreatment of the cells with staurosporine.
中性粒细胞通过触发呼吸爆发和产生毒性自由基来降解吞噬的日本脑炎(JE)病毒粒子的能力已得到研究。日本脑炎病毒(JEV)或JEV诱导的巨噬细胞衍生因子(MDF)通过激活胞质NADPH并随后形成过氧化氢,诱导细胞内氧化信号增加并产生超氧阴离子(O2-),在感染后第7天活性最高。该反应对抗MDF抗体治疗敏感。此外,研究揭示了吞噬的JE病毒蛋白和核酸的快速降解。病毒蛋白降解部分依赖于毒性氧物种的产生,因为用星形孢菌素预处理细胞可消除这种降解。