Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

The hepatitis C virus now infects 170 million people worldwide. The majority of infected people develop viral persistence that may lead to increasing liver fibrosis, liver cirrhosis, and hepatocellular cancer. Interferon therapy has been the mainstay of treatment for hepatitis C since the discovery of the virus in 1989. The introduction of a pegylated form of interferon that increases the half-life of interferon, and the concurrent use of ribavirin has significantly improved the likelihood of achieving long-term viral eradication. HCV genotype and viral load remain major determinants of response to interferons. However, very recently, host genetic polymorphisms linked to interferon-λ3 have also been shown to play a crucial role in clinical outcome. A significant body of evidence now exists showing that the hepatitis C virus has developed multiple strategies to subvert both the production and the antiviral effects of interferons. This review explores these strategies, the factors that determine the effectiveness of interferon therapy, and highlights novel interferons in development. Ultimately, given the significant side effect profile of interferon therapy, and the emergence of small molecules and therapeutic vaccines that may inhibit viral replication, the aim will be to achieve viral eradication without interferon treatment. © 2010 Rajoriya and Barnes, publisher and licensee Dove Medical Press Ltd.


Journal article


International Journal of Interferon, Cytokine and Mediator Research

Publication Date





85 - 95