Immune responses in hepatitis C: is virus or host the problem?

Hepatitis C virus is an RNA virus that usually establishes persistent infection in its host. As an important cause of cirrhosis and hepatocellular carcinoma worldwide, hepatitis C is a growing public health concern. Despite recent advances in therapy, most people infected with the virus can expect lifelong infection. In the minority of those exposed and who spontaneously clear virus, a robust hepatitis C virus-specific T cell response of T helper 1 type correlates with resolution. The longevity of this response in the recovered state and the potential for hepatitis C virus-specific T cells to protect against future infection are critical parameters for vaccine design.

The literature of the past year dissected components of protective immunity to hepatitis C and emphasized the importance of the CD4 helper response in both the expansion and maintenance of hepatitis C virus-specific CD8(+) T cells. Other important studies examined how the virus interacts with immune cells to subvert both innate and adaptive immune responses in acute and chronic infection.

Defining the essential components of protective immunity against a highly mutable virus like hepatitis C underpins successful vaccine design. By understanding viral and host factors which influence hepatitis C virus-specific T cell maintenance and function, we are better equipped to devise immunomodulatory therapies and vaccines which induce robust and lasting immunity.