(correction: officially, at least, hepatocytes only run on ketoacids (pyruvate and oxaloacetate) from amino acid catabolism. However, another reference (Best and Taylor) implies that these are fasting-state gluconeogenesis substrates, and states that the newborn liver is wholly dependent on sugars and lipids. It seems more likely that any cell uses a mix of energy substrates and that in the case of hepatocytes the preferential usage is ketoacids, if only because other cells cannot metabolize gluconeogenic amino acids. Anyhow, this suggestion can be left in the air for now.)
[update 10-12-2012: HCV infection can associated with a DROP in tryglycerides; see this recent post. The virus is monopolizing VLDL in the same way it monopolizes cholesterol.]
Because HCV down-regulates GLUT2 to produce the gluconeogenic effect, reducing glucose uptake of infected hepatocytes, fructose becomes an ideal substrate for both gluconeogenesis and lipogenesis. Fructose consumption is predicted to optimize viral replication.
More on Fructose:
This classic account is from White, Handler and Smith's Principles of Biochemistry (c) 1954, the 1973 edition