美國威斯康星大學(xué)的研究人員日前稱,，鳥類禽流感病毒和人類季節(jié)性流感病毒的雜交和相互作用有可能產(chǎn)生一種高致病性流感病毒,，其傳染能力甚至與H1N1病毒無異。研究人員在小鼠實驗中發(fā)現(xiàn),，H3N2人類季節(jié)性流感病毒基因中的一個片段能將H5N1禽流感病毒轉(zhuǎn)化為一種具有更高致病性的病毒類型,。相關(guān)研究2月22日發(fā)表在《美國科學(xué)院院刊》網(wǎng)絡(luò)版上。
根據(jù)世界衛(wèi)生組織的數(shù)據(jù),，通過候鳥和人類活動的傳播,，H5N1型禽流感病毒在全球已有442名確診病例，其中死亡病例已達(dá)262例,。
負(fù)責(zé)該研究的美國威斯康星大學(xué)麥迪遜分校病毒學(xué)教授河岡義裕稱,，H5N1病毒本身并不具備人際傳播能力，所以在人群中并未發(fā)生大流行,。但令人擔(dān)心的是,，通過雜交，目前遍及全球的H1N1病毒或許會為這種高致病性禽流感病毒提供在人際間傳播的能力,。當(dāng)這兩種病毒同時感染一個宿主細(xì)胞時,，其遺傳物質(zhì)將發(fā)生重組，重組后的毒株將兼具兩個親本病毒的特性,。
但在此之前,，科學(xué)家在實驗室中培育出的雜交病毒的毒性都小于親本病毒。新研究稱,，在H5N1病毒和H1N1病毒同時暴露的情況下,，兩種病毒極有可能雜交產(chǎn)生更具傳染性和致病性的新病毒，而且這種新病毒極有可能具備人際傳播能力,。
新的研究發(fā)現(xiàn),，病毒毒性的增加來自于一個被稱為PB2的基因片段，它由8個基因組成,，是禽流感病毒在人類等哺乳動物身上的宿主基因,。在小鼠實驗中，研究人員已經(jīng)檢測到了人類版本的PB2基因與H5N1高致病性禽流感病毒基因的交換行為,。
研究人員稱,，目前應(yīng)該加強對禽流感病毒和人類季節(jié)性流感病毒的監(jiān)測,，以及時發(fā)現(xiàn)它們的變種。他們的研究表明,，PB2基因片段是病毒毒性增強的一個重要標(biāo)志物,，可作為病毒監(jiān)測的參考。
河岡義裕說,，隨著H1N1流感病毒的大流行,，人們似乎已淡忘了H5N1禽流感病毒，但現(xiàn)實是這種病毒的威脅依然存在,。數(shù)據(jù)表明,，在H5病毒和大流行的H1N1病毒間極有可能發(fā)生重組，從而產(chǎn)生出一種更具傳染性的H5N1病毒,。(生物谷Bioon.com)
生物谷推薦原文出處：
PNAS doi: 10.1073/pnas.0912807107
Reassortment between avian H5N1 and human H3N2 influenza viruses creates hybrid viruses with substantial virulence
Chengjun Lia, Masato Hattaa,1, Chairul A. Nidomb,c, Yukiko Muramotod, Shinji Watanabea, Gabriele Neumanna, and Yoshihiro Kawaokaa,d,e,f,1
The spread of avian H5N1 influenza viruses around the globe has become a worldwide public health concern. To evaluate the pathogenic potential of reassortant viruses between currently cocirculating avian H5N1 and human H3N2 influenza viruses, we generated all the 254 combinations of reassortant viruses between A/chicken/South Kalimantan/UT6028/06 (SK06, H5N1) and A/Tokyo/Ut-Sk-1/07 (Tok07, H3N2) influenza viruses by reverse genetics. We found that the presence of Tok07 PB2 protein in the ribonucleoprotein (RNP) complex allowed efficient viral RNA transcription in a minigenome assay and that RNP activity played an essential role in the viability and replicative ability of the reassortant viruses. When the pathogenicity of 75 reassortant H5 viruses was tested in mice, 22 were more pathogenic than the parental SK06 virus, and three were extremely virulent. Strikingly, all 22 of these viruses obtained their PB2 segment from Tok07 virus. Further analysis showed that Tok07 PB1 alone lacked the ability to enhance the pathogenicity of the reassortant viruses but could do so by cooperating with Tok07 PB2. Our data demonstrate that reassortment between an avian H5N1 virus with low pathogenicity in mice and a human virus could result in highly pathogenic viruses and that the human virus PB2 segment functions in the background of an avian H5N1 virus, enhancing its virulence. Our findings highlight the importance of surveillance programs to monitor the emergence of human H5 reassortant viruses, especially those containing a PB2 segment of human origin.
