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Hepatitis C is a major public health challenge worldwide. It has evolved from a diagnosis of exclusion designated as “non-A, non-B hepatitis,”1 and principally associated with posttransfusion hepatitis, to an etiologically distinct disease; a major cause of cirrhosis, liver failure and hepatocellular carcinoma. The World Health Organization (WHO) estimates there are 71 million people infected with hepatitis C virus (HCV) worldwide, with 1,750,000 new infections in 2015 and about 400,000 deaths from the complications of infection.2 Others have estimated a much higher and increasing global prevalence, with 2.8% of the world’s population infected, translating to 185,000,000 infections, and substantially more disability and mortality than earlier estimates.3 The U.S. Centers for Disease Control and Prevention (CDC) notes that hepatitis C is now the leading cause of liver cancer and liver transplant in the United States, and that by 2013 the number of deaths associated with hepatitis C was greater than the mortality associated with 60 other nationally notifiable conditions combined.4


The identification of the hepatitis B virus led to the availability of serologic markers for hepatitis B, so that hepatitis C could be recognized as a form of “serum hepatitis” distinct from hepatitis B.5 The etiologic agent of hepatitis C was characterized only so far as it could be demonstrated to be transmissible and associated with chronic infection, particularly in posttransfusion hepatitis. It was differentiated from hepatitis A on the basis of epidemiological evidence and incubation period, as well as lack of serologic evidence of hepatitis A among cases.1

A putative antigen marker associated with non-A, non-B hepatitis was identified in 1979 using antibody in serum obtained from people who were convalescing from acute hepatitis. In 1989, Choo et al.,6 using blind recombinant immunoscreening, identified single-stranded RNA coding for an antigen in a patient with non-A, non-B hepatitis. The genetic sequences identified suggested that the virus was of the family Togoviridae or Flaviviridae. The genome was further characterized and was recognized to be a flavivirus (Flaviviridae) and was given the name HCV, eventually assigned to a new genus, Hepacivirus.7 HCV was once the only species in this genus, but closely related hepaciviruses have been identified in other primates, dogs, rodents, cows, bats, and even sharks, with the virus most closely related to human HCV being the equine hepacivirus.8

The HCV genome consists of single-stranded, positive-sense RNA of approximately 9.6 kilobases (kb). The genome is an open reading frame that codes a single polyprotein of approximately 3,000 amino acids that is cleaved into 10 protein products by cellular and viral proteases. The products include a core protein, two envelope surface glycopeptides (E1, E2), and nonstructural proteins designated p7, NS2, NS3, NS4A, NS4B, NS5A, and NS5B. The nonstructural proteins have a variety of enzymatic and replication functions; and have been the targets for therapeutic agents (see Table 158-1). ...

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