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首页> 外文期刊>Journal of Clinical Microbiology >Use of single-gene reassortant viruses to study the role of avian influenza A virus genes in attenuation of wild-type human influenza A virus for squirrel monkeys and adult human volunteers.
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Use of single-gene reassortant viruses to study the role of avian influenza A virus genes in attenuation of wild-type human influenza A virus for squirrel monkeys and adult human volunteers.

机译：使用单基因重配病毒研究A型禽流感病毒基因在减轻松鼠猴和成年人类志愿者的野生型A型流感病毒中的作用。

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The transfer of six internal RNA segments from the avian influenza A/Mallard/New York/6750/78 (H2N2) virus reproducibly attenuates human influenza A viruses for squirrel monkeys and adult humans. To identify the avian influenza A virus genes that specify the attenuation and host range restriction of avian-human (ah) influenza A reassortant viruses (referred to as ah reassortants), we isolated six single-gene reassortant viruses (SGRs), each having a single internal RNA segment of the influenza A/Mallard/New York/6750/78 virus and seven RNA segments from the human influenza A/Los Angeles/2/87 (H3N2) wild-type virus. To assess the level of attenuation, we compared each SGR with the A/Los Angeles/2/87 wild-type virus and a 6-2 gene ah reassortant (having six internal RNA segments from the avian influenza A virus parent and two genes encoding the hemagglutinin and neuraminidase glycoproteins from the wild-type human influenza A virus) for the ability to replicate in seronegative squirrel monkeys and adult human volunteers. In monkeys and humans, replication of the 6-2 gene ah reassortant was highly restricted. In humans, the NS, M, PB2, and PB1 SGRs each replicated significantly less efficiently (P less than 0.05) than the wild-type human influenza A virus parent, suggesting that each of these genes contributes to the attenuation phenotype. In monkeys, only the NP, PB2, and possibly the M genes contributed to the attenuation phenotype. These discordant observations, particularly with regard to the NP SGR, indicate that not all genetic determinants of attenuation of influenza A viruses for humans can be identified during studies of SGRs conducted with monkeys. The PB2 and M SGRs that were attenuated in humans each exhibited a new phenotype that was not observed for either parental virus. Thus, it was not possible to determine whether avian influenza virus PB2 or M gene itself or a specific constellation of avian and human influenza A virus specified restriction of virus replication in humans.
机译：从禽流感A / Mallard / New York / 6750/78（H2N2）病毒中转移六个内部RNA片段可再现地减弱了松鼠猴和成年人类的人类甲型流感病毒。为了鉴定指定甲型人流感（A）重组流感病毒（简称ah重组株）的减毒和寄主范围限制的禽流感A病毒基因，我们分离了六种单基因重组病毒（SGR），每个都有一个流感A / Mallard / New York / 6750/78病毒的一个内部RNA片段和人流感A / Los Angeles / 2/87（H3N2）野生型病毒的七个RNA片段。为了评估减毒水平，我们将每种SGR与A / Los Angeles / 2/87野生型病毒和6-2基因ah重配子（具有来自禽流感A病毒亲本的六个内部RNA片段和两个编码野生型人类甲型流感病毒的血凝素和神经氨酸酶糖蛋白），以在血清阴性的松鼠猴和成年人类志愿者中复制。在猴子和人类中，高度限制了6-2基因ah重配体的复制。在人类中，NS，M，PB2和PB1 SGRs的复制效率均显着低于野生型人类甲型流感病毒亲本（P小于0.05），这表明这些基因中的每一个都有助于减毒表型。在猴子中，只有NP，PB2以及可能的M基因有助于减毒表型。这些不一致的观察结果，特别是关于NP SGR的观察结果表明，在与猴子进行的SGR研究中，并非所有能确定人类A型流感病毒减毒的遗传决定因素。在人类中减毒的PB2和M SGRs均表现出一种新的表型，而这两种亲本病毒均未观察到。因此，不可能确定禽流感病毒PB2或M基因本身或禽和人类甲型流感病毒的特定星座是否规定了人类病毒复制的限制。

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