MRC Human Immunology Unit, WIMM, University of Oxford, OX3 9DS, UK; CAMS Oxford Institute, Nuffield Department of Medicine, Oxford University, OX3 9FZ, UK.
MRC Human Immunology Unit, WIMM, University of Oxford, OX3 9DS, UK; CAMS Oxford Institute, Nuffield Department of Medicine, Oxford University, OX3 9FZ, UK.
Biomed J. 2019 Feb;42(1):19-26. doi: 10.1016/j.bj.2019.01.004. Epub 2019 Mar 20.
The role of host genetics in influenza infection is unclear despite decades of interest. Confounding factors such as age, sex, ethnicity and environmental factors have made it difficult to assess the role of genetics without influence. In recent years a single nucleotide polymorphism, interferon-induced transmembrane protein 3 (IFITM3) rs12252, has been shown to alter the severity of influenza infection in Asian populations. In this review we investigate this polymorphism as well as several others suggested to alter the host's defence against influenza infection. In addition, we highlight the open questions surrounding the viral restriction protein IFITM3 with the hope that by answering some of these questions we can elucidate the mechanism of IFITM3 viral restriction and therefore how this restriction is altered due to the rs12252 polymorphism.
尽管人们对宿主遗传学在流感感染中的作用感兴趣已有数十年,但仍不清楚其作用机制。年龄、性别、种族和环境等混杂因素使得在不受影响的情况下评估遗传学的作用变得困难。近年来,研究表明,干扰素诱导跨膜蛋白 3(IFITM3)的单核苷酸多态性 rs12252 改变了亚洲人群流感感染的严重程度。在这篇综述中,我们研究了这种多态性以及其他一些被认为可以改变宿主对流感感染防御的多态性。此外,我们还强调了围绕病毒限制蛋白 IFITM3 的悬而未决的问题,希望通过回答其中的一些问题,我们能够阐明 IFITM3 对病毒的限制机制,以及由于 rs12252 多态性如何改变这种限制。