Hepatitis C virus (HCV) affects many people each year and presents a challenge for liver transplant patients. The infection caused by the virus mainly affects the liver and has a higher prevalence in Africa and Asia. Furthermore, there is currently no vaccination against this virus and the virus spreads via blood-to-blood contact. While it seems like we are helpless against an HCV infection, that may soon be changing. In a recent article published in PLoS Pathogens, scientists have identified a potential therapy. Not only does this therapy offer the hope of treating a HCV infection, it could also allow us to think about new strategies for treating other infections.
The research focuses on the fundamental mechanism by which viruses take over the host cells. The virus particles essentially hijack the host cell's lipid metabolism and promote the excessive production of lipids, leading to the formation of intracellular organelles called lipid droplets. The excessive production of lipids provides a favorable environment for lipids to multiply. In this study, the researchers focus on the master regulator of cholesterol pathway—subtilisin/kexin-isozyme-1 (SKI-1)—or site-1 protease (S1P). SKI-1/S1P controls the enzymes regulating fatty acid metabolism and lipid synthesis required for the formation of lipid droplets. They show that inhibiting this enzyme not only reduces the synthesis of neutral lipids and lipid droplets but also blocks HCV infection in hepatoma cells. Rather than target the virus itself, which is constantly mutating, the researchers targeted the host cell and created conditions that would be unsuitable for the virus to replicate.
Developing antiviral drugs has been a challenge because of the rapid mutation rate of the virus. The current discovery opens up new avenues for developing therapies for combating HCV infection. But there is much more promise to this approach — many viruses hijack the host cells lipid pathways to cause an infection. It may very well be that targeting the host cell's lipid metabolism may be the key to developing a whole new class of antiviral therapies.