Department of Molecular Biology, Princeton University, Princeton, NJ, USA.
Autophagy. 2009 Aug;5(6):870-1. doi: 10.4161/auto.9046. Epub 2009 Aug 19.
Autophagy is acknowledged as an important cellular defense mechanism against intracellular pathogens. As with other innate immune responses, pathogens have adapted to evade autophagy and in some cases, subvert the pathway to promote their own replication. Poliovirus, a prototypical small positive-strand RNA virus that replicates and assembles in the cytoplasm of the host cell, utilizes membranes derived from the autophagic pathway to aid viral replication and egress from the cell. Recently we made the surprising discovery that GFP-LC3-staining vesicles are physically immobilized during poliovirus infection. Here we discuss our model for the mechanism of vesicle immobilization and the predictions it makes for pathogens that subvert the autophagic pathway to their own ends.
自噬被认为是一种重要的细胞防御机制，可抵御细胞内病原体。与其他先天免疫反应一样，病原体已经适应了逃避自噬，并在某些情况下颠覆该途径以促进自身复制。脊髓灰质炎病毒是一种典型的小正链 RNA 病毒，在宿主细胞的细胞质中复制和组装，利用来自自噬途径的膜来辅助病毒复制和从细胞中逸出。最近，我们令人惊讶地发现，GFP-LC3 染色小泡在脊髓灰质炎病毒感染期间被物理固定。在这里，我们讨论了我们对小泡固定机制的模型，以及它对那些颠覆自噬途径以达到自身目的的病原体的预测。
