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. 2011 Dec 2;6(12):e28551. doi: 10.1371/journal.pone.0028551

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This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.

This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration, which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

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Replication of HCV RNA and production of HCV structural (core, E1, E2, and p7) and non-structural proteins (NS2, NS3, NS4A, NS4B, NS5A, and NS5B) in the rough ER and the subsequent partition of HCV proteins to different subcellular compartments lead to ER stress, mitochondrial injury, and the production of ROS. These cytopathic effects lead to activation of autophagy without a concomitant increase in protein degradation. Consequently, autophagosomes accumulate in HCV infected cells. EM photo with normal mitochondria (M) and rough ER (RER) was taken from healthy Huh7 cells; EM photos with enlarged mitochondria, ER blebbing, lipid droplet (L), and autophagosomes (A) were taken from genome-length and subgenomic replicon cells. The HCV genetic materials contained in genome-length replicon, subgenomic replicon, and Core-on cells are depicted at the top of the diagram.