Letter to the editor
Epstein-Barr virus infection is not associated with islet cell and insulin auto-antibody seroconversion
Dear Sir, We have been longitudinally studying first-degree relatives of insulin-dependent diabetic patients, for the appearance of islet cell (ICA) and insulin (IAA) auto-antibodies. Overall we have observed 26 such seroconversion events mostly in early childhood [1]. Some of these children have shown very convincing seroconversion under the age of 3 years over an observation period of less than 1.2 years, and it is likely that the appearance of these antibodies signals an event related to the onset of immune destruction of the islets. This serological signal may be more closely related in time to the latter event than the appearance of clinical diabetes, which may not occur until many years later.
Several authors [2-5] have suggested that Epstein-Barr virus (EBV) infection may be the triggering event, particularly as the virus infection at an early age may be silent, yet subsequently latent or persistent. EBV shares a pentapeptide code with the non-aspartate DOff 57 HLA marker associated with diabetes [2] and antibodies to this pentapeptide (GPPAA) appear in parallel with EBV nuclear antibodies after acute infection.
Therefore, the sera of 5 children under the age of 3 years (from this overall group of 26), who have shown a gross change in both ICA and IAA status over a period of i year, have been examined for EBV nuclear antibodies (Table 1). Subsequently two of these children developed diabetes.
As can be seen in Table 1, no child showed evidence of previous EBV infection before or after ICA seroconversion. It is thus unlikely that EBV infection is a common initiating event for the immunological cascade which may eventually result in diabetes. This method of relating viral infection to islet-related auto-antibody seroconversion may have application in studying the role of other viruses which have been implicated in the aetiopathogenesis of insulin-dependent diabetes.