Potapova Oxana V, Sharkova Tatyana V, Shkurupiy Vyacheslav A, Shestopalov Alexander M
FSBI Research Center of Clinical and Experimental Medicine, SB RAMS, Timakova Street 2, Novosibirsk 630117, Russia.
Clin Dev Immunol. 2013;2013:342686. doi: 10.1155/2013/342686. Epub 2013 Dec 23.
Highly pathogenic avian influenza H5N1 (HPAI H5N1) viruses can infect mammals, including humans, causing severe systemic disease with the inhibition of the immune system and a high mortality rate. In conditions of lymphoid tissue depletion, the liver plays an important role in host defence against viruses. The changes in mice liver infected with HPAI H5N1 virus A/goose/Krasnoozerskoye/627/05 have been studied. It has been shown that the virus persistence in the liver leads to the expression of proinflammatory cytokines (TNF- α , IL-6) and intracellular proteases (lysozyme, cathepsin D, and myeloperoxidase) by Kupffer cells. Defective antiviral response exacerbates destructive processes in the liver accelerating the development of liver failure.
高致病性禽流感H5N1(HPAI H5N1)病毒可感染包括人类在内的哺乳动物,引发严重的全身性疾病,抑制免疫系统并导致高死亡率。在淋巴组织耗竭的情况下,肝脏在宿主抗病毒防御中发挥重要作用。研究了感染HPAI H5N1病毒A/鹅/克拉斯诺亚尔斯克oye/627/05的小鼠肝脏变化。结果表明,病毒在肝脏中的持续存在导致库普弗细胞表达促炎细胞因子(TNF-α、IL-6)和细胞内蛋白酶(溶菌酶、组织蛋白酶D和髓过氧化物酶)。抗病毒反应缺陷加剧了肝脏中的破坏过程,加速了肝衰竭的发展。