意大利科學(xué)家近日表示,，他們找到了病毒如何改變?nèi)祟?lèi)進(jìn)化歷程的證據(jù),。他們?cè)?39個(gè)基因中發(fā)現(xiàn)了400多種不同的變異,，這些基因變異對(duì)人們是否容易感染病毒至關(guān)重要,。該項(xiàng)研究成果發(fā)表在《公共科學(xué)圖書(shū)館—遺傳學(xué)》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(lái)自全球不同地區(qū)的52個(gè)人種的基因組,，這些地區(qū)均遭遇了人類(lèi)在20萬(wàn)年的進(jìn)化過(guò)程中出現(xiàn)過(guò)的病毒,。
科學(xué)家早就知道，病毒影響了人類(lèi)的基因組,。研究已經(jīng)證明,，8%的基因組由所謂的內(nèi)源性逆轉(zhuǎn)錄病毒組成。
科學(xué)家仔細(xì)研究了這52個(gè)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(rèn)為這是一種找到同病毒有關(guān)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(gè)基因在人類(lèi)的進(jìn)化過(guò)程中被挑選出來(lái),，其中某些基因會(huì)使得人類(lèi)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(rùn)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?；A(chǔ)”的階段，還需要進(jìn)行重復(fù)測(cè)試,。不過(guò),，研究人員表示，該發(fā)現(xiàn)將幫助科學(xué)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(wú)傷地度過(guò)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(lèi)進(jìn)化過(guò)程
人類(lèi)進(jìn)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.
