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The prevalence of serum antibodies to hepatitis C virus was assessed by an enzyme-linked immunosorbent assay in patients with epidemic non-A, non-B hepatitis (14), sporadic non-A, non-B hepatitis (42), chronic hepatitis (14) and cirrhosis (26). None of the patients with epidemic non-A, non-B hepatitis (14) and acute self-limiting sporadic non-A, non-B hepatitis without prior parenteral exposure (38) tested positive for hepatitis C virus antibody. Based on epidemiologic features, hepatitis E virus is presumably the etiologic agent for both these entities. Hepatitis C virus (HCV) antibody was positive in none of the patients with cryptogenic chronic hepatitis (11) and in 2(8%) patients with cryptogenic cirrhosis (25). It was concluded that cryptogenic chronic hepatitis and cirrhosis in India may be caused by alternative viral agents of the non-A, non-B type or by hepatotoxins to which the population may be exposed. Of 8 patients with prior parenteral exposure (transfusions 6, needle pricks 2) 5 (62.5%) patients tested positive for HCV antibody. HCV antibody was detected in 1 (25%) patient with acute self-limiting, parenterally transmitted non-A, non-B hepatitis and in 4 (100%) patients with chronic parenterally transmitted non-A, non-B hepatitis.

Hepatitis E virus (HEV) causes an enteric non-A, non-B hepatitis. The disease occurs in epidemic settings and sporadically, and viral transmission is thought to be faecal-oral. We present here a single volunteer study of HEV transmission followed by disease. Clinical and biochemical features of the infection correlated with HEV detection in the stools and sera by reverse transcription/polymerase chain amplification. IgG antibody has persisted for 2 years. The presence of HEV in serum before clinical signs appeared suggests that in endemic areas sporadic transmission of HEV may also occur parenterally.