Institute of Medical Virology, University of Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland.
Institute of Medical Virology, University of Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland.
Cell Rep. 2017 Sep 12;20(11):2538-2546. doi: 10.1016/j.celrep.2017.08.061.
Host restriction of influenza A virus limits pandemic emergence. The viral RNA polymerase (vPol) is an essential enzyme that must adapt for avian viruses to replicate in humans. Species differences in host ANP32A dictate adaptation: human ANP32A lacks an uncharacterized 33 amino-acid insertion that is present in avian ANP32A. Here, we uncover important contributions of host SUMOylation to vPol activity, including avANP32A function. We also identify a hydrophobic SUMO interaction motif (SIM)-like sequence unique to avANP32A that critically supports avian-signature vPol. Unrelated SIM sequences partially recapitulate this function when introduced into huANP32A. By investigating ANP32A-vPol interactions, we find that huANP32A interacts weakly with both human- and avian-signature vPols, while the hydrophobic motif of avANP32A promotes stronger interactions. Furthermore, we identify a highly acidic stretch in avANP32A that constitutes a major site of vPol interaction. Our data suggest compensatory mechanisms underlying vPol adaptation to host ANP32A independent of species-specific interactions.
宿主对甲型流感病毒的限制限制了大流行的出现。病毒 RNA 聚合酶(vPol)是一种必需的酶,它必须适应禽流感病毒在人体内的复制。宿主 ANP32A 的种间差异决定了适应性:人 ANP32A 缺乏一个未被描述的 33 个氨基酸插入,而该插入存在于禽 ANP32A 中。在这里,我们揭示了宿主 SUMOylation 对 vPol 活性的重要贡献,包括 avANP32A 的功能。我们还鉴定了一个独特的 avANP32A 中的疏水性 SUMO 相互作用基序 (SIM)-样序列,该序列对禽源 vPol 的功能至关重要。当将非相关的 SIM 序列引入 huANP32A 时,该序列部分重现了这一功能。通过研究 ANP32A-vPol 相互作用,我们发现 huANP32A 与人类和禽源 vPol 均弱相互作用,而 avANP32A 的疏水性基序则促进了更强的相互作用。此外,我们鉴定出 avANP32A 中的一段高度酸性延伸,这是 vPol 相互作用的主要位点。我们的数据表明,vPol 适应宿主 ANP32A 的补偿机制独立于种间相互作用。