Hepatitis C virus and lipid droplets: finding a niche

• Lipid droplet storage organelles are crucial for the assembly of infectious HCV virions.
• Two viral proteins, core and NS5A, target lipid droplets.
• Virus assembly is linked to production of very low density lipoprotein.
• HCV infection is linked to steatosis – the accumulation of lipid droplets.
• The virus likely deregulates the lipid biosynthesis pathway.

Hepatitis C virus (HCV) causes serious liver disease in chronically infected individuals. Infectious virions are released from hepatocytes as lipoprotein complexes, indicating that the virus interacts with very low density lipoprotein (VLDL) assembly to propagate. The primary source of lipid for incorporation into VLDL is cytoplasmic lipid droplets (LDs). This organelle is targeted by two virus-encoded proteins as part of a process essential for virion morphogenesis. Moreover, LDs regulate infection. A common condition in HCV-infected individuals is steatosis, characterized by an accumulation of LDs. The mechanisms underlying development of steatosis include direct effects of the virus on lipid metabolism. This review reveals new insights into HCV infection and a further twist to the growing list of functions performed by LDs.