意大利科學家近日表示,，他們找到了病毒如何改變人類進化歷程的證據,。他們在139個基因中發(fā)現(xiàn)了400多種不同的變異，這些基因變異對人們是否容易感染病毒至關重要,。該項研究成果發(fā)表在《公共科學圖書館—遺傳學》雜志上,。
意大利米蘭“住院病人治療和研究中心”的研究人員分析了來自全球不同地區(qū)的52個人種的基因組，這些地區(qū)均遭遇了人類在20萬年的進化過程中出現(xiàn)過的病毒,。
科學家早就知道,，病毒影響了人類的基因組。研究已經證明,，8%的基因組由所謂的內源性逆轉錄病毒組成,。
科學家仔細研究了這52個人種的基因組，并將發(fā)現(xiàn)的感染與基因變異聯(lián)系在一起,，他們認為這是一種找到同病毒有關的基因的好辦法,。他們發(fā)現(xiàn),，感染多種不同病毒的人種的基因變異更多。研究人員表示,，這139個基因在人類的進化過程中被挑選出來,，其中某些基因會使得人類更容易或更不容易感染病毒。研究人員也發(fā)現(xiàn),，非洲某些溫暖濕潤的地區(qū)可為病毒提供很好的生存環(huán)境,。
該研究工作目前尚處于“非常基礎”的階段,，還需要進行重復測試,。不過，研究人員表示,，該發(fā)現(xiàn)將幫助科學家研發(fā)出更好的藥物和疫苗,，也有助于解釋為什么有些人能夠毫發(fā)無傷地度過流感季節(jié)而有些人卻很容易感染病毒。(生物谷Bioon.com)
PNAS：新方法有望呈現(xiàn)人類進化過程
人類進化的難題
生物谷推薦原文出處：
PLoS Genetics doi:10.1371/journal.pgen.1000849
Genome-Wide Identification of Susceptibility Alleles for Viral Infections through a Population Genetics Approach
Matteo Fumagalli1,2, Uberto Pozzoli1, Rachele Cagliani1, Giacomo P. Comi3, Nereo Bresolin1,3, Mario Clerici4,5#, Manuela Sironi1#*
1 Scientific Institute IRCCS E. Medea, Bioinformatic Lab, Bosisio Parini (LC), Italy, 2 Bioengineering Department, Politecnico di Milano, Milan, Italy, 3 Dino Ferrari Centre, Department of Neurological Sciences, University of Milan, IRCCS Ospedale Maggiore Policlinico, Mangiagalli and Regina Elena Foundation, Milan, Italy, 4 Department of Biomedical sciences and Technologies LITA Segrate, University of Milan, Milan, Italy, 5 Don C. Gnocchi ONLUS Foundation IRCCS, Milan, Italy
Viruses have exerted a constant and potent selective pressure on human genes throughout evolution. We utilized the marks left by selection on allele frequency to identify viral infection-associated allelic variants. Virus diversity (the number of different viruses in a geographic region) was used to measure virus-driven selective pressure. Results showed an excess of variants correlated with virus diversity in genes involved in immune response and in the biosynthesis of glycan structures functioning as viral receptors; a significantly higher than expected number of variants was also seen in genes encoding proteins that directly interact with viral components. Genome-wide analyses identified 441 variants significantly associated with virus-diversity; these are more frequently located within gene regions than expected, and they map to 139 human genes. Analysis of functional relationships among genes subjected to virus-driven selective pressure identified a complex network enriched in viral products-interacting proteins. The novel approach to the study of infectious disease epidemiology presented herein may represent an alternative to classic genome-wide association studies and provides a large set of candidate susceptibility variants for viral infections.
