Over 170 million people are infected with the hepatitis C virus worldwide, resulting in a large disease burden and significant mortality. Hepatitis C virus is rarely cleared in the acute phase of the infection and most patients become chronically infected; a proportion of these patients develop progressive liver disease and fibrosis. The outcome of infection depends on the immune responses of both the innate and cognate immune systems, and these in turn are orchestrated by networks of cytokines and chemokines. There is evidence that a vigorous type 1 immune response to viral proteins is required for viral elimination, and the recruitment of such effector cells to the liver is dependent on the local activity of specific inducible chemokines. Multiple factors determine the ability of the hepatitis C virus to survive host immune responses, including an ability to alter the cytokine profile secreted by T cells and to cause resistance to the effects of antiviral cytokines such as interferon. In the present review, we briefly cover the important advances made in this area over the past 12 months.