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本文引用的文献

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Inflammasomes as mediators of immunity against influenza virus.炎性小体作为抵抗流感病毒免疫的介质。
Trends Immunol. 2011 Jan;32(1):34-41. doi: 10.1016/j.it.2010.11.004. Epub 2010 Dec 14.
2
The lower serum immunoglobulin G2 level in severe cases than in mild cases of pandemic H1N1 2009 influenza is associated with cytokine dysregulation.2009年甲型H1N1流感重症病例的血清免疫球蛋白G2水平低于轻症病例,这与细胞因子失调有关。
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Profiles of cytokine and chemokine gene expression in human pulmonary epithelial cells induced by human and avian influenza viruses.人及禽流感病毒诱导的人肺上皮细胞细胞因子和趋化因子基因表达谱。
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Chemokine receptor 5 △32 allele in patients with severe pandemic (H1N1) 2009.严重大流行(H1N1)2009 患者的趋化因子受体 5 △32 等位基因。
Emerg Infect Dis. 2010 Oct;16(10):1621-2. doi: 10.3201/eid1610.100108.
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Host adaptive immunity deficiency in severe pandemic influenza.严重大流行流感中的宿主适应性免疫缺陷。
Crit Care. 2010;14(5):R167. doi: 10.1186/cc9259. Epub 2010 Sep 14.
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The 2009 A (H1N1) influenza virus pandemic: A review.2009 年甲型 H1N1 流感大流行:综述。
Vaccine. 2010 Jul 12;28(31):4895-902. doi: 10.1016/j.vaccine.2010.05.031. Epub 2010 May 27.
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Significance of the myxovirus resistance A (MxA) gene -123C>a single-nucleotide polymorphism in suppressed interferon beta induction of severe acute respiratory syndrome coronavirus infection.甲型流感病毒耐药 A 基因 -123C>a 单核苷酸多态性对严重急性呼吸综合征冠状病毒感染中干扰素β诱导抑制的意义。
J Infect Dis. 2010 Jun 15;201(12):1899-908. doi: 10.1086/652799.
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Influenza virus activates inflammasomes via its intracellular M2 ion channel.流感病毒通过其细胞内的 M2 离子通道激活炎症小体。
Nat Immunol. 2010 May;11(5):404-10. doi: 10.1038/ni.1861. Epub 2010 Apr 11.
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Severity of 2009 pandemic influenza A (H1N1) virus infection in pregnant women.孕妇感染 2009 年大流行性流感 A(H1N1)病毒的严重程度。
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10
What is the evidence of a role for host genetics in susceptibility to influenza A/H5N1?宿主遗传学在易感性方面对甲型 H5N1 流感的作用有何证据?
Epidemiol Infect. 2010 Nov;138(11):1550-8. doi: 10.1017/S0950268810000518. Epub 2010 Mar 18.

与人畜共患H1N1和H5N1流感病毒引起的严重呼吸道疾病相关的免疫遗传因素。

Immunogenetic factors associated with severe respiratory illness caused by zoonotic H1N1 and H5N1 influenza viruses.

作者信息

Juno Jennifer, Fowke Keith R, Keynan Yoav

机构信息

Department of Medical Microbiology, University of Manitoba, Winnipeg, MB, Canada R3E 0J9.

出版信息

Clin Dev Immunol. 2012;2012:797180. doi: 10.1155/2012/797180. Epub 2011 Nov 3.

DOI:10.1155/2012/797180
PMID:22110538
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3216312/
Abstract

Following the 2009 H1N1 pandemic and ongoing sporadic avian-to-human transmission of H5N1 viruses, an emphasis has been placed on better understanding the determinants and pathogenesis of severe influenza infections. Much of the current literature has focused on viral genetics and its impact on host immunity as well as novel risk factors for severe infection (particularly within the H1N1 pandemic). An understanding of the host genetic determinants of susceptibility and severe respiratory illness, however, is currently lacking. By better defining the role of genetic variability in influenza infection and identifying key polymorphisms that impair the host immune response or correlate with protection, we will be able to better identify at-risk populations and new targets for therapeutic interventions and vaccines. This paper will summarize known immunogenetic factors associated with susceptibility or severity of both pH1N1 and H5N1 infections and will also identify genetic pathways and polymorphisms of high relevance for future study.

摘要

在2009年甲型H1N1流感大流行以及H5N1病毒持续从禽类向人类散发传播之后,人们开始着重更好地了解严重流感感染的决定因素和发病机制。当前的许多文献都聚焦于病毒遗传学及其对宿主免疫的影响,以及严重感染的新风险因素(尤其是在甲型H1N1流感大流行期间)。然而,目前尚缺乏对宿主遗传易感性决定因素和严重呼吸道疾病的了解。通过更好地界定遗传变异性在流感感染中的作用,并确定损害宿主免疫反应或与保护作用相关的关键多态性,我们将能够更好地识别高危人群,并确定治疗干预措施和疫苗的新靶点。本文将总结已知的与甲型H1N1流感和H5N1感染的易感性或严重性相关的免疫遗传因素,并确定对未来研究具有高度相关性的遗传途径和多态性。