SUMMARY Twelve serologically proven cases of non-A, non-B (NANB) hepatitis have been described. The clinical course was mild in 11 patients. One patient, however, presented in portal systemic encephalopathy and required steroid treatment. Nine of the 12 patients continued to exhibit raised transaminase (AST) activities six or more months after the onset of the acute hepatitis. In these immunoglobulin concentrations were normal and autoantibodies were not present in significant titre. Four patients had evidence of previous hepatitis B infection, suggesting that the route of transmission of NANB might be similar to that of hepatitis B virus. A further four patients gave a history which suggests a possible parenteral mode of transmission. Liver biopsies were carried out both in the acute (8 cases) and chronic (6 cases) phases of the disease. Histological findings in liver biopsies covered the whole spectrum of acute and chronic hepatitis and 1 patient had cirrhosis. One notable feature in these biopsies was the presence of fatty changes.

SUMMARY Ten cases are reported of short incubation (one to four weeks) non-A, non-B hepatitis occurring after infusion of various preparations of factor VIII concentrates into patients with coagulation disorders. Five patients were symptomatic and, in all, serum transaminase levels were increased for at least six months. These cases of chronic hepatitis exhibited none of the features of autoimmune chronic hepatitis: autoantibodies were negative and serum immunoglobulins were normal. Hepatic histology confirmed acute hepatitis in two cases biopsied early in the illness, and thronic active hepatitis (three) or chronic persistent hepatitis (two) in five cases studied later. Lobular inflammation was a prominent feature in all cases. Other features not commonly associated with type A or B hepatitis included fatty change and damaged bile ducts.Patients with congenital coagulation disorders receive large quantities of blood derivatives and acute hepatitis is not an uncommon occurrence.

SUMMARY Delta antigen (6) is a transmissible agent requiring hepatitis B virus (HBV) for its replication. Antibody to 6 (anti-b) was present in nine of 71 (13%) British HBV carriers: six were intravenous drug abusers and two were haemophiliacs. Anti-6 was negative in 30 HBsAg positive homosexuals. Cirrhosis was common in patients with anti-6 and those with anti-6 positive cirrhosis were significantly younger than those with anti-6 negative cirrhosis. In British HBV carriers 6 infection is associated with intravenous drug abuse and haemophilia and perhaps a more rapid progression of chronic liver disease.Delta antigen (6) was discovered by direct immunofluorescence in hepatocyte nuclei of Italian patients with chronic hepatitis B virus (HBV) infection; it is distinct from other HBV antigens. ' Hepatitis B virus carriers with 6 in the liver have a serum antibody (anti-b) in high titre detectable by radioimmunoassay and 6 itself has been extracted from liver and serum.2-4 Delta antigen from liver is a protein of 68 000 daltons.2 In serum it is associated with a low molecular weight RNA encapsulated by hepatitis B surface antigen (HBsAg) in a 35-37 nm subpopulation of particles.3 4Studies in chimpanzees suggest that 6 is a marker of a transmissible pathogenic agent, either a variant of HBV or another virus which requires HBV for its replication.5 6 Anti-b is prevalent in Italian HBV carriers and more common in patients with chronic liver disease.7 The prevalence of anti-6 in British HBV carriers is unknown. The aim of this study was to determine whether 6 infection is common in British HBV carriers and its significance in terms of predicting the severity of chronic liver disease. Methods PATIENTSSeventy one HBsAg carriers born and resident in Great Britain were studied. Sixty four men and seven women; mean age 36 years (range 11-67 years). Forty five were HBeAg and 26 anti-HBe

ABSTRACT— Liver biopsies from 17 patients with serologically established hepatitis A were examined by light microscopy. Biopsies were taken from 2 to 27 weeks after onset of symptoms. All showed acute hepatitis, usually with centrilobular lesions but also commonly with a striking portal and periportal inflammatory reaction, resembling that seen in chronic active hepatitis. The infiltrate was rich in plasma cells. Centrilobular cholestasis was common and occasionally severe. Neither cholestasis nor the periportal lesion appeared to be related to patient age or to the timing of liver biopsy. All patients made a full recovery and none developed chronic liver disease. The histological changes differed from those reported in children and in chimpanzees in the presence of centrilobular lesions, but resembled them in that the latter two groups also had periportal lesions. These lesions may lead to a false impression of impending chronicity if the aetiology of the hepatitis is not known at the time of liver biopsy.

Non-A, non-B (NANB) viral hepatitis was successfully transmitted to two colony-born Tamarins following inoculation with antihaemophilic factor VIII concentrate or the "H" inoculum. Both animals showed histological and ultrastructural evidence of viral hepatitis, with raised alanine aminotransferase (ALT) levels from the second week after inoculation through to the end of follow-up, 5 months later.