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Nature:基因差异可影响人类抗流感能力

来源:新华网 2012-03-26 22:54

在2009年的甲型H1N1流感大流行中,有的感染者病情严重,有的仅出现轻微症状。英国和美国的研究人员3月25日联合发表研究报告说,人体内一个基因的“版本”不同影响了人们抵抗流感的能力。

根据这篇3月25日在线发表于《Nature》杂志网站上的文章,该基因名为IFITM3,它会指导合成与它同名的蛋白质。最开始研究人员发现这种蛋白质能在试管中抑制流感病毒的复制,于是通过动物实验进行验证。

结果发现,那些这一基因被技术性剔除的实验鼠,由于缺少相关蛋白质,即使只感染低致病性的流感病毒,也会出现较严重的症状,但如果重新引入这个基因,则症状会随之减轻。

研究人员分析了人类所携带的这个基因后发现,人体的这个基因存在两个版本。本次研究报告作者之一、英国桑格研究所的薛雅丽博士说,虽然两个版本的基因只有一处小小的不同,但它们指导合成的蛋白质在功能上却大不相同,其结果就是感染同样的流感病毒,有的人病情会特别严重,有的人却只有轻微症状。

对流感患者的分析也显示,无论是甲型H1N1流感,还是普通的季节性流感,那些病情较重的患者往往都携带了对病毒抵抗力较弱的那个基因版本。

薛雅丽说,这项研究成果对防治流感来说有重要意义,如果再出现大规模流感疫情,医疗卫生部门可以通过基因检测手段,预先筛查出那些对流感病毒抵抗力较弱的人群,有针对性地注射疫苗或采取其他防护措施,降低死亡率。此外从长远看,这项研究结果也有助开发新的流感药物和治疗手段。(生物谷 bioon.com)

IFITM3 restricts the morbidity and mortality associated with influenza

Aaron R. Everitt, Simon Clare, Thomas Pertel, Sinu P. John, Rachael S. Wash, Sarah E. Smith, Christopher R. Chin, Eric M. Feeley, Jennifer S. Sims, David J. Adams, Helen M. Wise, Leanne Kane, David Goulding, Paul Digard, Verneri Anttila, J. Kenneth Baillie, Tim S. Walsh, David A. Hume, Aarno Palotie, Yali Xue, Vincenza Colonna, Chris Tyler-Smith, Jake Dunning, Stephen B. Gordon, The GenISIS Investigators et al.

The 2009 H1N1 influenza pandemic showed the speed with which a novel respiratory virus can spread and the ability of a generally mild infection to induce severe morbidity and mortality in a subset of the population. Recent in vitro studies show that the interferon-inducible transmembrane (IFITM) protein family members potently restrict the replication of multiple pathogenic viruses1, 2, 3, 4, 5, 6, 7. Both the magnitude and breadth of the IFITM proteins’ in vitro effects suggest that they are critical for intrinsic resistance to such viruses, including influenza viruses. Using a knockout mouse model8, we now test this hypothesis directly and find that IFITM3 is essential for defending the host against influenza A virus in vivo. Mice lacking Ifitm3 display fulminant viral pneumonia when challenged with a normally low-pathogenicity influenza virus, mirroring the destruction inflicted by the highly pathogenic 1918 ‘Spanish’ influenza9, 10. Similar increased viral replication is seen in vitro, with protection rescued by the re-introduction of Ifitm3. To test the role of IFITM3 in human influenza virus infection, we assessed the IFITM3 alleles of individuals hospitalized with seasonal or pandemic influenza H1N1/09 viruses. We find that a statistically significant number of hospitalized subjects show enrichment for a minor IFITM3 allele (SNP rs12252-C) that alters a splice acceptor site, and functional assays show the minor CC genotype IFITM3 has reduced influenza virus restriction in vitro. Together these data reveal that the action of a single intrinsic immune effector, IFITM3, profoundly alters the course of influenza virus infection in mouse and humans.

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