Shkurupy V A, Potapova O V, Sharkova T V, Shestopalov A M, Troitskii A V
Research Center of Clinical and Experimental Medicine, Siberian Division of the Russian Academy of Medical Sciences, Novosibirsk, Russia.
Bull Exp Biol Med. 2015 Feb;158(4):483-8. doi: 10.1007/s10517-015-2790-3. Epub 2015 Feb 24.
Intranasal infection of outbred male mice with influenza A/H5N1 A/goose/Krasnoozerskoye/627/05 virus led to high (85%) mortality of animals. Morphological studies of liver specimens showed destructive changes in the parenchyma (93.5% hepatocytes), caused by long persistence of the virus in the liver. The virus persistence was conjugated with activation of cellular immunity, manifesting by an increase in the counts of cells with high expression of proinflammatory cytokines (TNF-α) and lysosomal enzymes (lysozyme, cathepsin D). Injections of oxidized dextran 3 and 1 days before infection reduced mortality and 2-fold attenuated destructive changes in the liver, presumably due to prevention of virus penetration into the target cells, modulation of immune reactions, and stimulation of reparative plastic processes.
用甲型H5N1 A/鹅/克拉斯诺奥泽尔斯克oye/627/05病毒对远交系雄性小鼠进行鼻内感染,导致动物出现高死亡率(85%)。肝脏标本的形态学研究显示,实质组织出现破坏性变化(93.5%的肝细胞),这是由病毒在肝脏中长期持续存在所致。病毒持续存在与细胞免疫激活相关,表现为促炎细胞因子(TNF-α)和溶酶体酶(溶菌酶、组织蛋白酶D)高表达细胞数量增加。在感染前3天和1天注射氧化葡聚糖可降低死亡率,并使肝脏的破坏性变化减轻2倍,这可能是由于防止病毒侵入靶细胞、调节免疫反应以及刺激修复性再生过程。