美国威斯康星大学的研究人员日前称，鸟类禽流感病毒和人类季节性流感病毒的杂交和相互作用有可能产生一种高致病性流感病毒，其传染能力甚至与H1N1病毒无异。研究人员在小鼠实验中发现，H3N2人类季节性流感病毒基因中的一个片段能将H5N1禽流感病毒转化为一种具有更高致病性的病毒类型。相关研究2月22日发表在《美国科学院院刊》网络版上。
根据世界卫生组织的数据，通过候鸟和人类活动的传播，H5N1型禽流感病毒在全球已有442名确诊病例，其中死亡病例已达262例。
负责该研究的美国威斯康星大学麦迪逊分校病毒学教授河冈义裕称，H5N1病毒本身并不具备人际传播能力，所以在人群中并未发生大流行。但令人担心的是，通过杂交，目前遍及全球的H1N1病毒或许会为这种高致病性禽流感病毒提供在人际间传播的能力。当这两种病毒同时感染一个宿主细胞时，其遗传物质将发生重组，重组后的毒株将兼具两个亲本病毒的特性。
但在此之前，科学家在实验室中培育出的杂交病毒的毒性都小于亲本病毒。新研究称，在H5N1病毒和H1N1病毒同时暴露的情况下，两种病毒极有可能杂交产生更具传染性和致病性的新病毒，而且这种新病毒极有可能具备人际传播能力。
新的研究发现，病毒毒性的增加来自于一个被称为PB2的基因片段，它由8个基因组成，是禽流感病毒在人类等哺乳动物身上的宿主基因。在小鼠实验中，研究人员已经检测到了人类版本的PB2基因与H5N1高致病性禽流感病毒基因的交换行为。
研究人员称，目前应该加强对禽流感病毒和人类季节性流感病毒的监测，以及时发现它们的变种。他们的研究表明，PB2基因片段是病毒毒性增强的一个重要标志物，可作为病毒监测的参考。
河冈义裕说，随着H1N1流感病毒的大流行，人们似乎已淡忘了H5N1禽流感病毒，但现实是这种病毒的威胁依然存在。数据表明，在H5病毒和大流行的H1N1病毒间极有可能发生重组，从而产生出一种更具传染性的H5N1病毒。
生物谷推荐原文出处：
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.
