• HCV is the only member of the Hepacivirus genus within the Flaviviridae family.
• HCV is a +sense, ssRNA virus with an enveloped, icosahedral capsid 30-60 nm in diameter.
• Currently, 7 genotypes have been reported, with genotype 1 the most common cause of HCV infection in the USA (70-75%). Determining the genotype is important as it can have therapeutic and prognostic implications.
• HCV is found worldwide, but is especially prevalent in Africa, the Middle East, Central and East Asia. For example, 1-2% of the population in the USA is infected, while approximately 15-20% of the population in Egypt is infected.
• HCV is transmitted primarily by percutaneous or mucosal contact with infectious blood and/or body fluids. In the USA, i.v. drug use is the primary mode of transmission now that blood and blood products are screened for HCV. Sexual and perinatal transmission is a much less frequent mode of transmission.
• The high incidence of chronic, asymptomatic infection promotes the spread of this virus.
• HCV only infects humans and chimpanzees.
• HCV invades hepatocytes in a very complex, multi-step process involving several cell surface receptors.
• HCV causes acute or chronic hepatitis, rarely fulminant hepatitis.
• The RNA polymerase of the virus is error prone generating mutations that lead to antigenic variability. Such variability makes the development of a vaccine difficult.
• Cell mediated immune responses are responsible for the resolution of the infection as well as tissue damage.
• HCV-specific antibody is not protective; therefore, a person may be reinfected.
• The incubation period averages 4-12 weeks (range 2-24 weeks).
• Acute hepatitis: 70-80% of persons infected will have mild to asymptomatic disease. Symptoms include: low grade fever, jaundice, fatigue, abdominal pain and dark urine, clay colored stools, and nausea /vomiting.
• Chronic Hepatitis: Symptoms may be mild to severe: 70-85% of HCV positive persons become chronically infected; 60-70% will develop chronic liver disease; 5-10% will develop cirrhosis and 1-5% will die from consequences of HCV infection (liver cancer or cirrhosis).
• Screening: The detection of antibody by enzyme immunoassay (EIA) may occur by 4-6 weeks postinfection, with a 97% sensitivity at 6 months postinfection. Reactivity in screening tests should be confirmed as false positives do occur.
• Confirmatory testing: Molecular techniques that detect HCV RNA in serum/plasma samples. If HCV RNA is not detected, confirmatory HCV-specific antibody tests are available.
Other viruses including HAV, HBV, HDV, HGV, HEV, CMV, EBV, Coxsackie and Yellow Fever virus; noninfectious causes of hepatitis (toxins, drug-induced)
• See Infectious Disease Society of America (IDSA) or American Association for the Study of Liver Diseases (AASLD) guidelines for current recommendations as HCV therapy is rapidly evolving. In addition to alpha-interferon and ribavirin, several new classes of direct-acting antivirals have been developed and FDA approved.
Prevention and control:
• Blood and blood products have been screened for HCV since 1990.
• No vaccine is available.
• Avoid behaviors that increase the risk of HCV infection (especially i.v. drug use).
• Limit the consumption of alcohol as it exacerbates the liver damage caused by HCV