In the United Kingdom and United States of America, fulminant viral hepatitis is due mainly to sporadic (non-parenteral) non-A, non-B hepatitis and hepatitis B whereas that caused by hepatitis A virus is very uncommon and by the herpes viruses remains rare. Recent advances in fulminant non-A, non-B hepatitis have come with the identification and cloning of a virus (27-34 nm) in the enteral variety (hepatitis E) which is prevalent in the Indian sub-continent, North Africa and elsewhere, especially in pregnant women. Virus-like particles (50-70 nm) with ultrastructural features similar to the togaviridae and flaviviridae have been identified in some patients with fulminant non-A, non-B hepatitis in the United Kingdom. The relation to hepatitis C virus, recently identified as a major cause of chronic post-transfusion (parenteral) non-A, non-B hepatitis, awaits serological analysis. The recent demonstration that persistence of active viral replication can occur in some cases of fulminant hepatitis types A and B using monoclonal antibody and molecular biology techniques challenges the classical views on the pathogenesis of these varieties of fulminant viral hepatitis.