Department of Virology, Tohoku University Graduate School of Medicine, 2-1 Seiryou-machi Aoba-ku, Sendai 980-8575, Japan.
Infect Genet Evol. 2010 May;10(4):569-74. doi: 10.1016/j.meegid.2010.01.010. Epub 2010 Feb 1.
In April 2009, pandemic H1N1/09 influenza, which originated from swine influenza, appeared in North America, and it has since spread globally among humans. It is important to know how swine influenza A virus broke the host barrier to cause a pandemic. We analyzed 673 strains of human, avian, and swine influenza viruses and assessed the internal genes PB2, PB1, PA, NP, M, and NS. Here we found accumulation of mutations in segments that were retained as well as introduced due to genetic reassortment of viruses. The retained segments may have to mutate to accommodate new segments. The mutations caused by interaction among segments retained and introduced due to reassortment between swine influenza viruses may have increased the adaptation of the virus to humans, leading to pandemic H1N1/09. We indicate the sites that probably contributed to the acquisition of efficient human-to-human transmission.
2009 年 4 月,起源于猪流感的甲型 H1N1 流感出现在北美,并已在全球范围内传播。了解猪流感 A 病毒如何突破宿主屏障引起大流行非常重要。我们分析了 673 株人流感、禽流感和猪流感病毒,并评估了内部基因 PB2、PB1、PA、NP、M 和 NS。在这里,我们发现保留的和由于病毒遗传重配而引入的片段中积累了突变。保留的片段可能需要突变以适应新的片段。由于猪流感病毒之间的重配而保留和引入的片段之间的相互作用引起的突变可能增加了病毒对人类的适应性,导致了甲型 H1N1/09 流感大流行。我们指出了可能有助于获得有效人际传播的位点。