Puzis L E, Lozitsky V P
I. I. Mechnikov Research Institute of Virology and Epidemiology, Odessa, U.S.S.R.
Acta Virol. 1988 Nov;32(6):515-21.
Proteolysis system was examined in influenza-virus-infected mice after a 5-day course of therapeutic or preventive treatments with the proteolysis inhibitor epsilon-aminocaproic acid (E-ACA). The mice were infected with nonadapted influenza virus A/Hong Kong/1/68 (H3N2). E-ACA was shown to exert a pathogenetic action expressed by a marked tendency to normalization of elevated alkaline protease activity in damaged lung tissue and in the blood of infected animals. E-ACA induced a long-lasting high level activity of acidic proteases in the blood which correlated with increased protection of animals against influenza virus infection. It may be suggested that acidic proteases are involved in the preventive action of E-ACA and are a factor of resistance to virus infection.
在用蛋白水解抑制剂ε-氨基己酸(E-ACA)进行5天疗程的治疗或预防处理后,对感染流感病毒的小鼠的蛋白水解系统进行了检查。小鼠感染了未适应的甲型流感病毒A/香港/1/68(H3N2)。结果显示,E-ACA具有致病作用,表现为受损肺组织和感染动物血液中升高的碱性蛋白酶活性有显著恢复正常的趋势。E-ACA诱导血液中酸性蛋白酶产生持久的高水平活性,这与动物对流感病毒感染的保护作用增强相关。可以推测,酸性蛋白酶参与了E-ACA的预防作用,并且是抵抗病毒感染的一个因素。