Abstract
Introduction One unusual characteristic of HCV is to establish chronic infection and the precise mechanisms remain unclear. Materials and methods Huh-7 cells were transiently transfected with E2 and subjected to MTT assay, DNA fragmentation assay, and Western blotting to see the impact of E2 protein on apoptosis. Results and discussion E2 may inhibit cell proliferation by inducing apoptosis and pro-caspases 3, 8, and 9 were cleaved and activated to result in the presence of active forms in a time-dependent fashion, which suggest that E2-induced apoptosis is caspase-dependent. Furthermore, the cytosolic level of cytochrome c was increased together with a gradually down-regulated Bcl-2 and up-regulated Bax protein expression. The continuing reduction of Bid protein and the gradual increase of tBid protein also indicated that a time-dependent increased turn-over of Bid protein into tBid. Taken together, our data suggested that HCV E2 may induce apoptosis through a mitochondrial damage-mediated caspase pathway.
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