Abstract
To the Editor: Current evidence indicates that post-transfusion hepatitis still occurs in 11 per cent of transfusion recipients, despite sensitive testing of donor serum samples for hepatitis B surface antigen (HBsAg).1 At least 90 per cent of these cases are attributed to non-A, non-B viruses, which cause considerable morbidity. Intensive searches for useful markers to detect non-A, non-B viruses in donor blood have been unsuccessful.Although their causes are distinct, type B and non-A, non-B hepatitis have clinical and epidemiologic features in common, including the core antigen–antibody system.2 Recent studies have demonstrated that hepatitis B virus sequences were integrated into . . .