Hepatitis C Virus The term non-A, non-6 (NANB) hepatitis has been used for the past decade or so to include those acute hepatitic illnesses that clearly are not related to infection with hepatitis A virus, hepatitis B virus, cytomegalovirus, or Epstein-Barr virus. NANB hepatitis accounts for an estimated 150,000 cases yearly in the United States, of which 5% to 10% are transfusion-related; 40% are associated with intravenous drug abuse; 5%, with occupational (health care) exposure; and lo%, with heterosexual activity with multiple partners, or household and/or sexual contact with an individual with hepatitis. Forty percent are without an identifiable source of infection. It has been clearly established that a prolonged NANB hepatitis carrier state develops frequently and, more importantly, that chronic hepatitis may develop in about half of patients with NANB hepatitis. Twenty percent of the latter group progress to cirrhosis. In addition, NANB hepatitis may be causally related to hepatocellular carcinoma and to sporadic community-acquired hepatitis. Until recently, attempts to identify a specific viral agent that could be associated with significant numbers of cases of NANB hepatitis had been frustrating and unsuccessful. Choo and associates, using techniques of modern molecular biology and working with sera capable of transmitting NANB hepatitis to primates, isolated a cDNA clone derived from the genome of a blood-borne NANB hepatitis agent.’ This agent, the hepatitis C virus (HCV), is thought to be an RNA virus, probably related to the togaviruses or flaviviruses. An assay for measuring antibodies to this agent was quickly developed,2 and there has been a veritable explosion of related knowledge. It has already been established that HCV is the major cause of posttransfusion NANB hepatitis. Screening of blood donors for antibody to HCV should prevent the majority of such cases and has recently been instituted. In addition, HCV appears to be the etiologic agent of up to 90% of sporadic, community-acquired NANB hepatitis that occurs in patients without a history of parenteral exposure. Studies of sera from patients in Italy and Japan, as well as from those in the United States, have confirmed HCV as a major cause of NANB hepatitis worldwide. Development of anti-HCV antibody is delayed, being first detected an average of 22 weeks after transfusion, or some 15 weeks after onset of clinical hepatitis. It is important to note that some patients do not become seropositive for anti-HCV until as long as 1 year after infection. 3 In patients with chronic liver disease, antiHCV has persisted, but in patients with acute resolving hepatitis, anti-HCV disappeared after approximately 4 years. Treatment trials that utilized interferon alfa for patients with chronic hepatitis C have shown promising results.4 We can expect much additional data to be generated in the next few years to elucidate more fully the impact of HCV. A readily available diagnostic test for anti-HCV has been developed and is now widely available.