Imperial College London, Faculty of Medicine, Division of Infectious Disease, London, United Kingdom.
J Virol. 2013 Jan;87(2):1278-84. doi: 10.1128/JVI.02597-12. Epub 2012 Oct 31.
Avian-origin influenza virus polymerase activity can be dramatically increased in human cells with the PB2 E627K mutation. Previously, others have proposed that this mutation increases the stability of the viral ribonucleoprotein complex (vRNP) measured by the interaction between PB2 and NP. However, we demonstrate here that a variety of PB2 adaptive mutations, including E627K, do not enhance the stability of the vRNP but rather increase the amount of replicated RNA that results in more PB2-NP coprecipitation.
禽类起源的流感病毒聚合酶活性在具有 PB2 E627K 突变的人类细胞中可以显著增加。此前,其他人提出,该突变通过 PB2 和 NP 之间的相互作用增加了病毒核糖核蛋白复合物(vRNP)的稳定性。然而,我们在这里证明,包括 E627K 在内的各种 PB2 适应性突变并不会增强 vRNP 的稳定性,而是会增加复制的 RNA 量,从而导致更多的 PB2-NP 共沉淀。