6. Conclusions
The effect of lipid metabolism on host-pathogen interactions has often been neglected in virology.
The unique interaction between HCV and lipid metabolism offers the opportunity to deeply investigate
the role of lipids in all the steps of the infectious cycle of a virus. The association of the viral particle
with apolipoproteins and neutral lipids affects the way HCV interacts with the host cell at the entry step
to generate a productive infection. Although the receptors and co-receptors of HCV are known, it is not
clear if and how the lipidic part of the particle changes in the different stages of the entry process. Viral
proteins induce profound changes in the intracellular membrane architecture and biochemical composition
assuring the environment for viral replication. The picture of lipid dynamics and effector recruitment
during the replication step is not complete and it awaits further development. Furthermore, viral assembly is
associated with LD, it strongly depends on apoE and the particle seems to follow a similar maturation
pathway as VLDL. However, the assembly step of infectious HCV particles leaves a series of aspects
not yet addressed: the endogenous factors involved in the core envelopment step, the following sequence
of events which lead to the formation of an infectious LVP and the molecular architecture of such a
peculiar virion. Importantly, further studies of the interaction between HCV and lipid metabolism may
also potentially help to better understand the role of some lipids in cell metabolism.