Liver disease resulting from Hepatitis C Virus (HCV) infection is a serious, worldwide health problem. HCV is endemic to central Africa and Southeast Asia and has probably existed for over 100,000 years in these locations [1]. However, during the 20th century it became a worldwide epidemic, currently infecting an estimated 170 million people or 3% of the world's population [2]. HCV is a blood-borne virus, and its increased prevalence in modern times results from the increased use of blood transfusions, or the use of improperly sterilized needles, either for medical procedures such as vaccination, or for the intravenous administration of illicit drugs. However, HCV was only identified, and its genome sequenced, in the late 1980s [3]. Since that time, diagnostic tests have essentially eliminated the virus from the blood supply [4]. Furthermore, awareness of HCV, as well as of HIV, has led to decreased transmission through unsterilized needles. Intravenous drug use remains the major mode of Hepatitis C transmission, still occurring with significant frequency in certain populations, for example in prisons [5].

Acute infection by HCV is usually asymptomatic and passes unnoticed [6, 7]. The immune system brings this initial infection under control, and in some cases is able to completely eliminate the virus. However, the virus possesses several mechanisms to evade the immune response, so that approximately 80% of people become chronically infected [8]. Further progression of the disease is slow, but most chronically infected individuals eventually develop liver fibrosis, which can then lead to cirrhosis with or without progression to hepatocellular carcinoma. End-stage liver disease and liver failure resulting from HCV infection are currently the major indications for liver transplant in the U.S. and Europe [9].The progression from chronic infection to cirrhosis is poorly understood, and the extent to which pathology is caused, either directly by the virus or as a consequence of the body's immune response, is the subject of some debate. Current therapies for HCV, as described below, work by stimulating the immune system. They are poorly tolerated and only partially effective. There is a significant need for new forms of treatment, and it has long been recognized that drugs specific for viral targets will play a critical role in combating the disease. The NS3 serine protease in particular was recognized as a prime target for intervention 12 years ago [10]. However, to this day no drugs directed against any viral target have reached the market or late-stage clinical trials. For reasons outlined below, development of anti-HCV drugs, and protease drugs in particular, has been slow and difficult. Progress against this target was last reviewed in this series in 2002 [11]. Here we will focus primarily on recently reported results. The last few years have seen a number of exciting developments in this field, holding out the hope that highly effective drugs directed against this target will be available in the not-too-distant future.

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