禽类和哺乳动物细胞中聚合酶活性的差异决定了流感病毒的宿主范围。
Differential polymerase activity in avian and mammalian cells determines host range of influenza virus.
作者信息
Gabriel G, Abram M, Keiner B, Wagner R, Klenk H-D, Stech J
机构信息
Institut fuer Virologie, Philipps-Universität Marburg, Hans-Meerwein-Str. 2, 35043 Marburg, Germany.
出版信息
J Virol. 2007 Sep;81(17):9601-4. doi: 10.1128/JVI.00666-07. Epub 2007 Jun 13.
Abstract
As recently shown, mutations in the polymerase genes causing increased polymerase activity in mammalian cells are responsible for the adaptation of the highly pathogenic avian influenza virus SC35 (H7N7) to mice (G. Gabriel et al., Proc. Natl. Acad. Sci. USA 102:18590-18595, 2005). We have now compared mRNA, cRNA, and viral RNA levels of SC35 and its mouse-adapted variant SC35M in avian and mammalian cells. The increase in levels of transcription and replication of SC35M in mammalian cells was linked to a decrease in avian cells. Thus, the efficiency of the viral polymerase is a determinant of both host specificity and pathogenicity.
摘要
最近的研究表明，在哺乳动物细胞中导致聚合酶活性增加的聚合酶基因突变，是高致病性禽流感病毒SC35（H7N7）适应小鼠的原因（G. Gabriel等人，《美国国家科学院院刊》102:18590 - 18595，2005年）。我们现在比较了SC35及其适应小鼠的变体SC35M在禽类和哺乳动物细胞中的mRNA、cRNA和病毒RNA水平。SC35M在哺乳动物细胞中转录和复制水平的增加与禽类细胞中的减少相关。因此，病毒聚合酶的效率是宿主特异性和致病性的一个决定因素。
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