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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Lack of transmission of H5N1 avian-human reassortant influenza viruses in a ferret model
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Lack of transmission of H5N1 avian-human reassortant influenza viruses in a ferret model

机译：在雪貂模型中缺乏H5N1禽-人类重配流感病毒的传播

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摘要

Avian influenza A H5N1 viruses continue to spread globally among birds, resulting in occasional transmission of virus from infected poultry to humans. Probable human-to-human transmission has been documented rarely, but H5N1 viruses have not yet acquired the ability to transmit efficiently among humans, an essential property of a pandemic virus. The pandemics of 1957 and 1968 were caused by avian-human reassortant influenza viruses that had acquired human virus-like receptor binding properties. However, the relative contribution of human internal protein genes or other molecular changes to the efficient transmission of influenza viruses among humans remains poorly understood. Here, we report on a comparative ferret model that parallels the efficient transmission of H3N2 human viruses and the poor transmission of H5N1 avian viruses in humans. In this model, an H3N2 reassortant virus with avian virus internal protein genes exhibited efficient replication but inefficient transmission, whereas H5N1 reassortant viruses with four or six human virus internal protein genes exhibited reduced replication and no transmission. These findings indicate that the human virus H3N2 surface protein genes alone did not confer efficient transmissibility and that acquisition of human virus internal protein genes alone was insufficient for this 1997 H5N1 virus to develop pandemic capabilities, even after serial passages in a mammalian host. These results highlight the complexity of the genetic basis of influenza virus transmissibility and suggest that H5N1 viruses may require further adaptation to acquire this essential pandemic trait.
机译：甲型H5N1禽流感病毒继续在鸟类中全球传播，导致病毒偶尔从受感染的家禽传播给人类。可能的人对人传播很少有文献记载，但是H5N1病毒尚未获得在人间有效传播的能力，这是大流行性病毒的基本特征。 1957年和1968年的大流行是由具有人病毒样受体结合特性的禽人重组流感病毒引起的。然而，人们对人类内部蛋白质基因或其他分子变化对流感病毒在人类之间的有效传播的相对贡献仍然知之甚少。在这里，我们报告了一个比较性的雪貂模型，该模型与H3N2人类病毒的有效传播和H5N1禽流感病毒在人类中的传播较差相似。在此模型中，具有禽病毒内部蛋白基因的H3N2重配病毒表现出有效的复制，但传播效率低下，而具有四个或六个人病毒内部蛋白基因的H5N1重配病毒表现出复制减少且无传播。这些发现表明，单独的人类病毒H3N2表面蛋白基因不能提供有效的传播能力，即使是在哺乳动物宿主中连续传代后，单独获得人类病毒内部蛋白基因也无法使这种1997 H5N1病毒产生大流行能力。这些结果突出说明了流感病毒可传播性的遗传基础的复杂性，并表明H5N1病毒可能需要进一步适应才能获得这种基本的大流行性状。

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