In 1989, the Centers for Disease Control (CDC) and a California biotechnology firm collaborated to identify the hepatitis C virus as the causal agent in an outbreak of silent post transfusion hepatitis leading to cirrhosis. The HCV genome is now known to be a 9.6 kb single-stranded RNA. A single open reading frame encodes a 3011 amino acid residue polyprotein, which is proteolyzed to generate 10 distinct gene products, 3 structural proteins and 7 nonstructural (NS) proteins that engage in post translational proteolytic processing and replication of HCV genetic material. In less than 25 years, a new class of medicines called direct-acting antivirals (DAAs) that target these proteins was developed to treat HCV infection. These extremely powerful antiviral medicines are now licensed for treatment in children as young as three years old, with sustained virologic responses surpassing 90% in the majority of genotypes. Despite great scientific advances, the prevalence of acute HCV infections has grown fourfold since 2005, exacerbated in the previous decade by an increase in opioid and intravenous drug use.

Unfortunately, the general public’s knowledge of this lethal hepatotropic virus is very restricted. If this virus is to be eliminated, patient education, advocacy, and counseling must accompany the availability of curative therapies for HCV infection.