Study on roles of human metapneumovirus accessory proteins in viral pathogenecity

本研究揭示了人偏肺病毒辅助蛋白M2-2的功能。首先，M2-2与病毒RNA聚合酶L结合，负调控病毒基因组的复制和转录。其次，M2-2可能作为干扰素（IFN）拮抗剂，抑制α IFN的产生。这种活性不依赖于对基因组复制和转录的抑制活性，并且归因于在以产生大量α IFN为特征的浆细胞样树突细胞中Toll样受体7/9依赖性信号传导的阻断。

The present study has uncovered the following functions of human metapneumovirus accessory protein M2-2. Firstly, M2-2 binds to viral RNA polymerase L and negatively regulates replication and transcription of viral genome. Secondly, M2-2 potentially serves as an interferon (IFN) antagonist that inhibits alpha IFN production. This activity is independent of the inhibitory activity against genome replication and transcription, and ascribed to the blockade of Toll-like receptor 7/9-dependent signaling in plasmacytoid dendritic cells characteristic of producing a large amount of alpha IFN.