Hepatitis C Virus Screening

Hepatitis C virus (HCV) is primarily transmitted through blood exposure. It is a single-stranded RNA flavivirus, distinguished by a low rate of recognized acute infection and a high rate of chronic infection that results in substantial morbidity and mortality over long periods of observation. Because most infections are asymptomatic, testing blood donors is critical.

Historically, any viral hepatitis that was not caused by hepatitis A or B viruses was referred to as non-A, non-B hepatitis, which in 1989 was discovered to be HCV. In 1987, anti-HBc was implemented and served as a surrogate marker for screening out donors with these nonspecific hepatidities. In addition, HIV high-risk behavior questions, especially those related to blood exposure and needle use, eliminated many donors at risk of HCV infection. In 1990, anti-HCV testing was implemented, followed by a much improved test in 1992. In 1999, nucleic acid testing (NAT) became available; subsequently residual risk of transfusion-transmitted HCV (TT-HCV) is estimated to be 1:1,800,000 units transfused.

In 2015, the CDC reported that in the United States, the number of acute cases of HCV has been increasing annually from 2010 through 2015, with an overall incidence rate of 0.8 cases per 100,000 ( https://www.cdc.gov/hepatitis/statistics/2015surveillance/index.htm ). The most common risk factor identified was intravenous drug use and occupational blood exposure from needlesticks.

Treatment of HCV infection is critical to improving long-term health outcomes particularly because of the major advancements that have been made in treatments. Previously, treatment consisted of pegylated interferon combined with oral doses of ribavirin. Since 2011, with the development of direct-acting antivirals targeting nonstructural proteins of HCV, use of a combination regimen of these agents has increased viral response rates to >90%.