Epidemiological investigations of HCV actually began with the realization that there was still a high frequency of PTH after exclusion of HAV, HBV (Prince et al., 1974; Alter et al., 1975), and other viral and toxic causes of hepatitis (Reesink & van der Poel, 1989). In the 1970s and early 1980s, the frequency of NANB PTH in different countries ranged from 2–11 per 1000 transfusions in the Netherlands and 3 per 1000 in England to 10–28 per 1000 in the United States and 23 per 1000 in Italy (Reesink & van der Poel, 1989). Among patients receiving transfusions, more than 80% of PTH was designated as NANB PTH, with 10–20% symptomatic in the acute phase. Additional observations showed about half of those with NANB PTH developed chronic hepatitis, and up to 20% of those with chronic hepatitis went on to develop cirrhosis. Cirrhosis was also shown to be an important risk factor for the appearance of HCC (Dienstag, 1983; Reesink & van der Poel, 1989). Among people with NANB PTH, more than 40% had a history of intravenous drug abuse and 5–10% had a history of possible or known occupational exposure to blood (mostly among health care providers). In addition to PTH, NANBH was also reported in up to 40% of those with acute sporadic hepatitis in the United States in which there was no history of blood transfusion (Alter et al., 1982).