To our Knowledge, only 2 cases of acute diabetes following an attack of infectious mononucleosis (IM) have previously been reported. The case described here thus represents the third such occurrence of acute diabetes, during the clinical course of Epstein-Barr (EB) virus infection.<BR>A 7-yr-old boy was admitted due to severe diabetic symptoms. Fifty days prior to admission, he had experienced vomiting and diarrhea followed by a fever of up to 39°C for 3 weeks. One week after these symptoms had subsided, he experienced severe polydipsia, polyuria, polyphagia and lost 3 kg of body weight. On admission he displayed systemic lymphnode enlargement and hepatomegaly. His laboratory data revealed leukocytosis (9700/mm³) with 3 % atypical lymphocytes, hyperglycemia (plasma glucose 600 mg/dl) and ketonemia (β-hydroxybutyrate 4296 μM). Serological analysis showed the Paul-Bunnell heterophile antibody test to be positive (1: 224) on admission and negative one month later. The immunofluorescence test for antibody to EB viral capsid antigen was at a titer of 1: 160 on admission, rose to as high as 1: 640 after 3 weeks and persisted at the same level for a further 3 months. The titer of IgM antibody for EB virus was 1: 640 on hospitalization, decreased to 1: 40 one month later and remained at the same level for the next 3 months. The patient's histocompatibility antigen was a phenotype of HLA-AW 26, BW 40/AW 24, B 7. The antibody against a microsomal component of thyroid cells appeared at the 7th month of diabetes. After successful treatment of the acute diabetes with insulin for one month, an oral glucose (O.75 g/kg body weight) tolerance test was performed. This demonstrated an almost total absence of immunoreactive insulin response. Subsequently, the patient has remained insulin dependent for more than 1 yr. He had no family history of diabetes and had not been obese. A urinary glucose test performed 1 yr before his admission was found to be negative by inquiring about his physical record at primary school.<BR>It is thus not likely that latent diabetes became overt due to the current infection. The time lag between the acute phase of IM and the onset of diabetes also opposes such occasional aggravation. In conclusion, therefore, the acute diabetes in the present case is considered to be newly induced by an irreversible injury of pancreatic B cells infected with EB virus.