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. 2010 Aug 24;2(8):1782–1803. doi: 10.3390/v2081782

Figure 2.

Figure 2.

Schematic representation of the assembly and release of HCV. Replication occurs at dedicated ER-derived membranes. Core and NS5A interact with lipid droplets and recruit the other non-structural proteins, and with them, the replication complex. Core and genomic RNA interact and oligomerize, and must interact with the envelope glycoproteins to form the viral particle. The viral particle interacts with the VLDL. VLDL assembly is depicted on the left side. ApoB interacts with triglycerides in an MTP-dependent manner to form a pre-VLDL, which will accumulate more lipids and ApoE in an MTP dependent process. Both the VLDL and the virus continue to undergo maturation during their passage through the secretory pathway. Red blocks mark potential drug targets in this process: (1) inhibition of the interaction of NS5A with LD or the other non-structural proteins, thus blocking their recruitment to LDs; (2) inhibition of NS2, a late stage block of assembly; (3) inhibition of p7 (BIT225 for example); (4) inhibition of the interaction of the core with LDs; (5) inhibition of the maturation of envelope proteins (inhibitors of α-glycosidases); (6) inhibition of core oligomerization and interaction with RNA; (7) inhibition of virus-VLDL association; (8) inhibition of VLDL secretion; (9) inhibition of VLDL formation from pre-VLDL targeting ApoE and MTP; (10) inhibition of the formation of pre-VLDL by the MTP dependent association of triglycerides with ApoB.