生物谷：黃熱病是一種烈性傳染性疾病,，埃及伊蚊（Aedes aegypti）是黃熱病傳播的罪魁禍?zhǔn)?。最近,，英?guó)帝國(guó)理工大學(xué)博士研究生Robert Waterhouse率領(lǐng)的研究小組首次完成了埃及伊蚊基因組的測(cè)序工作，并將伊蚊免疫系統(tǒng)的基因公布在22日出版的Science雜志,。
蚊蟲的免疫系統(tǒng)極具研究?jī)r(jià)值，在控制黃熱病病毒和登革熱病毒傳播中發(fā)揮關(guān)鍵作用,。此次Waterhouse等共鑒別出與免疫系統(tǒng)有關(guān)的350個(gè)基因,，發(fā)現(xiàn)這些基因比基因組其它基因的進(jìn)化速度快很多。之前,，他們已經(jīng)證實(shí),，其它蚊子的免疫系統(tǒng)或者允許或者阻止瘧疾寄生蟲傳播，至于新發(fā)現(xiàn)的埃及伊蚊基因是否有相似的抵抗致病病毒的機(jī)制,，需要進(jìn)一步研究,。影響這些基因的活性，有望幫助蚊子更有效擊退病毒,，切斷將病毒傳播到人類的環(huán)節(jié),。文章高級(jí)作者George Christophides博士說，更多地了解這些基因及它們與特異病原體相互作用的方式,，有望更全面了解病原體在昆蟲體內(nèi)生存的機(jī)制,。
Waterhouse等還將埃及伊蚊的免疫基因與果蠅,、瘧蚊的免疫基因進(jìn)行對(duì)比，發(fā)現(xiàn)埃及伊蚊和瘧蚊的有許多相似的免疫基因,，但也有許多不同,，于是打算下一步研究黃熱病傳播和瘧疾傳播的遺傳差異。Christophides博士說,，這項(xiàng)研究提示我們昆蟲的免疫系統(tǒng)不是靜止的,，而是有所差異且快速進(jìn)化的，可能原因是為了適應(yīng)各自遇到的病原體,。文章合作者Fotis Kafatos博士認(rèn)為,，弄清蚊子的病原體/免疫系統(tǒng)相互作用的遺傳機(jī)制有助于揭開特異種類蚊子攜帶特異致病病原體的機(jī)制。如果存在某種蚊子,，其沒有進(jìn)化出有效的抵抗病原體的免疫系統(tǒng),，我們有可能利用這些知識(shí)削弱其它蚊子的免疫系統(tǒng)的特異反應(yīng)，控制疾病的傳播,。
原始出處：
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* George Dimopoulos,4* Evgeny M. Zdobnov,3,19,1* George K. Christophides1*
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.
To whom correspondence should be addressed. E-mail: [email protected] (G.K.C.); [email protected] (E.M.Z.); [email protected] (F.C.K.)
