FIG 8.

Schematics illustrating the correlations between HBV and host cells. Global temporal quantitative proteomics analysis of long-term HBV-infected primary human hepatocytes accompanied by parallel transcriptomic analysis uncovered extensive remodeling of host proteome and transcriptome, as well as revealed cytopathic effects of long-term viral replication. Metabolic-, complement-, cytoskeleton-, mitochondrial-, and oxidation- related pathways were modulated at transcriptional or posttranscriptional levels, which could be partially rescued by early, but not late, nucleot(s)ide analogs therapy and could be relieved by RNAi. Thirteen proteins, many without characterized functions in promoting or inhibiting HBV replication, were identified by our unbiased analysis and further overexpression screen.