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从轻症和重症感染患者中分离出的禽流感 A(H7N9)病毒在致病性和细胞因子诱导方面存在差异。

Avian Influenza A (H7N9) viruses isolated from patients with mild and fatal infection differ in pathogenicity and induction of cytokines.

机构信息

Key Laboratory for Tropic Diseases Control of the Ministry of Education, Department of Microbiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, China.

Key Laboratory for Tropic Diseases Control of the Ministry of Education, Department of Microbiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, China; Teaching Center of Biology Experiment, Guangzhou Medical University, Guangzhou, 511436, China.

出版信息

Microb Pathog. 2017 Oct;111:402-409. doi: 10.1016/j.micpath.2017.08.022. Epub 2017 Aug 18.

Abstract

Since 2013, a novel Influenza A (H7N9) virus strain has continued to circulate within poultry and causing human disease. Influenza A (H7N9) virus results in two types of infection: mild and severe. The different results of clinical findings may be related with host susceptibility and characteristics of the virus itself. In order to investigate potential pathogenesis of Influenza A (H7N9) virus, we performed pathogenecity and cytokines analysis of two isolates, A/Guangdong/6/2013 H7N9 virus (GD-6) from a patient with a mild infection, and A/Guangdong/7/2013 H7N9 virus (GD-7) from a patient with a fatal infection. We found that GD-7 replicated to higher levels than GD-6 in human peripheral blood mononuclear cells (PBMCs), lung tissues, and mice. Furthermore, GD-7 infection resulted in more severe lung damage in mice lung tissues than GD-6 infection. GD-7 elicited higher levels of interleukin-6 (IL-6) and tumor necrosis factor-α(TNF-α) than GD-6 did. In conclusion, GD-7 was more pathogenic and induced higher levels of proinflammatory cytokines than GD-6 did.

摘要

自 2013 年以来,一种新型甲型流感(H7N9)病毒株一直在禽类中传播,并导致人类患病。甲型流感(H7N9)病毒导致两种类型的感染:轻度和重度。临床发现的不同结果可能与宿主易感性和病毒本身的特征有关。为了研究甲型流感(H7N9)病毒的潜在发病机制,我们对两株分离株(来自轻度感染患者的 A/广东/6/2013 H7N9 病毒[GD-6]和来自致命感染患者的 A/广东/7/2013 H7N9 病毒[GD-7])进行了致病性和细胞因子分析。我们发现,GD-7 在人外周血单核细胞(PBMCs)、肺组织和小鼠中复制的水平高于 GD-6。此外,GD-7 感染导致小鼠肺组织中的肺损伤比 GD-6 感染更为严重。GD-7 诱导的白细胞介素 6(IL-6)和肿瘤坏死因子-α(TNF-α)水平高于 GD-6。总之,GD-7 的致病性更强,诱导的促炎细胞因子水平高于 GD-6。

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