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一篇最新流感病毒文献摘要的翻译，同时求全文
大家好，小生在pubmed上查到一篇有关流感病毒的文献，可是只有摘要，如果有哪位大侠有全文可以共享，我将不胜感激。
以下是文献的摘要及我的翻译。因为水平实在有限，又在努力学英语中，所以翻译中肯定有很多不合适的地方，恳请大家帮我修改，或指出不足和个性意见。谢谢！
Proteases essential for human influenza virus entry into cells and their inhibitors as potential therapeutic agents.
Kido H, Okumura Y, Yamada H, Le TQ, Yano M.
Division of Enzyme Chemistry, Institute for Enzyme Research, The University of Tokushima, Kuramoto-cho 3-18-15, Tokushima 770-8503, Japan. kido@ier.tokushima-u.ac.jp
Influenza A virus (IAV) is one of the most common infectious pathogens in humans. Since IVA genome does not have the processing protease for the viral membrane fusion glycoprotein precursors, entry of this virus into cells is determined primarily by host cellular, trypsin-type, processing proteases that proteolytically activate the fusion glycoprotein precursors of IAV. At least five different processing proteases have been identified in the airways of animals and humans. These proteases determine the infectious organ tropism of IAV infection as well as the efficiency of viral multiplication in the airway, and sometimes in the brain. Proteases in the upper respiratory tract are suppressed by secretory leukoprotease inhibitor, and those in the lower respiratory tract are suppressed by pulmonary surfactant which, by adsorption, inhibits the interaction between the proteases and viral membrane proteins. Since protease activities predominate over those of endogenous inhibitory compounds under normal airway conditions, administration of protease inhibitors in the early-stage of infection significantly suppresses viral entry and viral multiplication. Several viral neuraminidase inhibitors are used clinically as anti-influenza virus agents, based on their inhibitory action on viral release from infected cells. Furthermore, protease inhibitors of viral entry could be potentially useful against influenza virus as well as neuraminidase inhibitor-resistant viruses. We also found that ambroxol, a mucolytic and anti-oxidant agent, up-regulates the levels of endogenous protease inhibitory compounds in the airway fluids in early-phase infection, and that clarithromycin, a macrolide antibiotic, increases IgA levels and mucosal immunity through augmentation of interleukin-12 levels in the airway. The combination of neuraminidase inhibitors and protease inhibitors, clarithromycin or ambroxol, could be potentially used as a potent anti-influenza therapy to minimize the emergence of drug-resistant mutant viruses.
A型流感病毒是人类最常见的感染原之一。因为IAV的基因组中没有编码处理病毒膜融合糖蛋白前体的加工蛋白酶的基因，所以病毒要进入细胞内部首先就要依靠宿主细胞的胰岛素样加工蛋白酶，此酶可以使IAV的膜融合糖蛋白水解。现在已经在人和动物的呼吸道上发现至少五种不同的加工蛋白酶。这些蛋白酶决定了IAV在何种组织中感染，同时也决定了病毒在呼吸道或是脑中增殖的效率。在上呼吸道中，这些蛋白酶被分泌型的白细胞蛋白酶抑制剂所抑制。而在下呼吸道则被肺表面活性物质所抑制。肺表面活性物质是通过在病毒吸附时阻止加工蛋白酶和病毒膜蛋白相互作用而起抑制作用的。既然，在人呼吸道中蛋白酶活化是内源性抑制剂复合物的主要部分，那么在感染的早期可以通过给予蛋白酶抑制剂的方法来抑制病毒的侵入和增殖。很多IAV的神经氨酸酶抑制剂被当作抗病毒药物用于临床，这是基于它可以抑制病毒从被感染的细胞中释放出来。此外，加工蛋白酶抑制剂可以用于神经氨酸酶抑剂抵抗的病毒感染时。我们同时发现，一种有粘液溶解作用的抗氧化剂―氨溴索可以在感染早期提高呼吸道分泌液中内源性蛋白酶抑制剂复合体的表达。而且还发现一种大环内酯类抗生素―克拉霉素可以通过增加呼吸道中IL-12的水平提高IgA表达和粘膜免疫。神经氨酶抑制剂和蛋白酶抑制剂同时应用，再加上克拉霉素或氨溴索可以在有效抗病毒治疗时使抗药病毒株出现的机率降到最低。再加上一篇，大家受累了！Role of host cytokine responses in the pathogenesis of avian H5N1 influenza viruses in mice.Szretter KJ, Gangappa S, Lu X, Smith C, Shieh WJ, Zaki SR, Sambhara S, Tumpey TM, Katz JM. Influenza Branch MS G-16, Division of Viral and Ricksettial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, 1600 Clifton Road NE, Atlanta, GA 30333, USA.Highly pathogenic avian H5N1 influenza viruses are now widespread in poultry in Asia and have recently spread to some African and European countries. Interspecies transmission of these viruses to humans poses a major threat to public health. To better understand the basis of pathogenesis of H5N1 viruses, we have investigated the role of proinflammatory cytokines in transgenic mice deficient in interleukin-6 (IL-6), macrophage inflammatory protein 1 alpha (MIP-1alpha), IL-1 receptor (IL-1R), or tumor necrosis factor receptor 1 (TNFR1) by the use of two avian influenza A viruses isolated from humans, A/Hong Kong/483/97 (HK/483) and A/Hong Kong/486/97 (HK/486), which exhibit high and low lethality in mice, respectively. The course of disease and the extent of virus replication and spread in IL-6- and MIP-1alpha-deficient mice were not different from those observed in wild-type mice during acute infection with 1,000 50% mouse infective doses of either H5N1 virus. However, with HK/486 virus, IL-1R-deficient mice exhibited heightened morbidity and mortality due to infection, whereas no such differences were observed with the more virulent HK/483 virus. Furthermore, TNFR1-deficient mice exhibited significantly reduced morbidity following challenge with either H5N1 virus but no difference in viral replication and spread or ultimate disease outcome compared with wild-type mice. These results suggest that TNF-alpha may contribute to morbidity during H5N1 influenza virus infection, while IL-1 may be important for effective virus clearance in nonlethal H5N1 disease.现在高致病性H5N1型禽流感病毒在亚洲的家禽中广泛传播，而且最近也传播到了非洲及欧洲的一些国家。禽到人的跨种间的病毒传播给人类的公共健康造成了主要威胁。为了更好的了解H5N1型流感病毒的致病基础，我们分别用从人类病人中分离得到的A/香港/483/97（HK/483）和A/香港/486/97（HK/486）两种病毒感染转基因小鼠，以研究致炎性细胞因子在流感病毒感染中的作用。这些转基因小鼠是IL-6，MIP-1alpha，IL-1受体缺失或是TNF受体1缺失的。而用于感染的两种病毒，前者对小鼠有高致死性，后者则只有低致死性。分别用两种50%致病剂量的H5N1型病毒感染IL-1和MIP-1alpha缺失的1000只小鼠，发现在急性感染期，这些小鼠的病程和病毒复制及传播与野生型的小鼠无差别。然而，用HK/486病毒感染IL-1受体缺失的小鼠时表现有高发病率和高致死率。而当用病性更强的HK/483病毒感染这种小鼠时并没有观察到明显的不同。此外，TNFR1缺失的小鼠在感染两种H5N1型病毒时发病率都显著降低，但是其病毒复制和传播及病终结局与野生型小鼠相比并无不同。这些结果显示：TNF-alpha可能对H5N1型流感病毒感染的发病起作用，而IL-1可能对非致命性的H5N1型病毒的清除有重要的影响。以上是我的翻译，其中有1000只小鼠的问题，我觉得太多了。是不是我理解错了啊？
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