Science：测序蚊虫免疫系统基因控制病毒传播

生物谷

    生物谷：黄热病是一种烈性传染性疾病，埃及伊蚊（Aedes  aegypti）是黄热病传播的罪魁祸首。最近，英国帝国理工大学博士研究生Robert  Waterhouse率领的研究小组首次完成了埃及伊蚊基因组的测序工作，并将伊蚊免疫系统的基因公布在22日出版的Science杂志。

    蚊虫的免疫系统极具研究价值，在控制黄热病病毒和登革热病毒传播中发挥关键作用。此次Waterhouse等共鉴别出与免疫系统有关的350个基因，发现这些基因比基因组其它基因的进化速度快很多。之前，他们已经证实，其它蚊子的免疫系统或者允许或者阻止疟疾寄生虫传播，至于新发现的埃及伊蚊基因是否有相似的抵抗致病病毒的机制，需要进一步研究。影响这些基因的活性，有望帮助蚊子更有效击退病毒，切断将病毒传播到人类的环节。文章高级作者George  Christophides博士说，更多地了解这些基因及它们与特异病原体相互作用的方式，有望更全面了解病原体在昆虫体内生存的机制。

    Waterhouse等还将埃及伊蚊的免疫基因与果蝇、疟蚊的免疫基因进行对比，发现埃及伊蚊和疟蚊的有许多相似的免疫基因，但也有许多不同，于是打算下一步研究黄热病传播和疟疾传播的遗传差异。Christophides博士说，这项研究提示我们昆虫的免疫系统不是静止的，而是有所差异且快速进化的，可能原因是为了适应各自遇到的病原体。文章合作者Fotis  Kafatos博士认为，弄清蚊子的病原体/免疫系统相互作用的遗传机制有助于揭开特异种类蚊子携带特异致病病原体的机制。如果存在某种蚊子，其没有进化出有效的抵抗病原体的免疫系统，我们有可能利用这些知识削弱其它蚊子的免疫系统的特异反应，控制疾病的传播。

原始出处：

Science 22 June 2007:
Vol. 316. no. 5832, pp. 1738 - 1743
DOI: 10.1126/science.1139862

Evolutionary Dynamics of Immune-Related Genes and Pathways in Disease-Vector Mosquitoes

Robert M. Waterhouse,1 Evgenia V. Kriventseva,2,3 Stephan Meister,1 Zhiyong Xi,4 Kanwal S. Alvarez,5 Lyric C. Bartholomay,6 Carolina Barillas-Mury,7 Guowu Bian,5 Stephanie Blandin,8 Bruce M. Christensen,9 Yuemei Dong,4 Haobo Jiang,10 Michael R. Kanost,11 Anastasios C. Koutsos,1 Elena A. Levashina,8 Jianyong Li,12 Petros Ligoxygakis,13 Robert M. MacCallum,1 George F. Mayhew,9 Antonio Mendes,1 Kristin Michel,1 Mike A. Osta,1 Susan Paskewitz,14 Sang Woon Shin,5 Dina Vlachou,1 Lihui Wang,13 Weiqi Wei,15,16 Liangbiao Zheng,15,17 Zhen Zou,10 David W. Severson,18 Alexander S. Raikhel,5 Fotis C. Kafatos,1* ${dagger}$ George Dimopoulos,4* Evgeny M. Zdobnov,3,19,1* ${dagger}$ George K. Christophides1* ${dagger}$

Mosquitoes are vectors of parasitic and viral diseases of immense importance for public health. The acquisition of the genome sequence of the yellow fever and Dengue vector, Aedes aegypti (Aa), has enabled a comparative phylogenomic analysis of the insect immune repertoire: in Aa, the malaria vector Anopheles gambiae (Ag), and the fruit fly Drosophila melanogaster (Dm). Analysis of immune signaling pathways and response modules reveals both conservative and rapidly evolving features associated with different functional gene categories and particular aspects of immune reactions. These dynamics reflect in part continuous readjustment between accommodation and rejection of pathogens and suggest how innate immunity may have evolved.

1 Division of Cell and Molecular Biology, Faculty of Natural Sciences, Imperial College London, London SW7 2AZ, UK.
2 Department of Structural Biology and Bioinformatics, University of Geneva Medical School, 1211 Geneva, Switzerland.
3 Department of Genetic Medicine and Development, University of Geneva Medical School, 1211 Geneva, Switzerland.
4 Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205, USA.
5 Department of Entomology and the Institute for Integrative Genome Biology, University of California, Riverside, CA 92521, USA.
6 Department of Entomology, Iowa State University, Ames, IA 50011, USA.
7 Laboratory of Malaria and Vector Research, Twinbrook III Facility, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD 20892–8132, USA.
8 CNRS Unité Propre de Recherche 9022, Avenir-Inserm, Institut de Biologie Moléculaire et Cellulaire, Strasbourg, France.
9 Department of Animal Health and Biomedical Sciences, University of Wisconsin-Madison, Madison, WI 53706, USA.
10 Department of Entomology and Plant Pathology, Oklahoma State University, Stillwater, OK 74078, USA.
11 Department of Biochemistry, Kansas State University, Manhattan, KS 66506, USA.
12 Department of Biochemistry, Virginia Tech, Blacksburg, VA 24061, USA.
13 Department of Biochemistry, University of Oxford, Oxford, UK.
14 Russell Labs, Department of Entomology, University of Wisconsin-Madison, Madison, WI 53706, USA.
15 Yale University School of Medicine, Epidemiology, and Public Health, New Haven, CT 06520, USA.
16 Fujian Center for Prevention and Control of Occupational Disease and Chemical Poisoning, Fujian, China.
17 Institute of Plant Physiology and Ecology, Shanghai, China.
18 Department of Biological Sciences, Center for Global Health and Infectious Diseases, University of Notre Dame, Notre Dame, IN46556, USA.
19 Swiss Institute of Bioinformatics, 1211 Geneva, Switzerland.

* These authors contributed equally to this work.

${dagger}$ To whom correspondence should be addressed. E-mail: g.christophides@imperial.ac.uk (G.K.C.); zdobnov@medecine.unige.ch (E.M.Z.); f.kafatos@imperial.ac.uk (F.C.K.)