Approximately 200 million people worldwide are persistently infected with the hepatitis C virus (HCV) and are at risk of developing chronic liver disease, cirrhosis and hepatocellular carcinoma. HCV can be treated using antiviral therapy, but the response to therapy is heterogeneous. Some patients clear infection, some patients remain chronically infected, and some patients exhibiting an intermediate plateau in viral load before clearing infection. One hypothesis for this diversity of therapy responses is that the homeostatic proliferation of hepatocytes may preserve infection through vertical transmission. In this talk, I will present some results of a mathematical analysis of the homeostasis hypothesis and discuss the implications.