Abstract
It has long been known that insulin-deficiency diabetes mellitus (IDDM) results from an inflammatory process of the islet tissue of the pancreas (insulitis), leading to essentially complete destruction of the insulin-producing beta cells. The factors responsible for this destructive process have been the focus of intense research by many investigators. Although the investigative roots go back at least 80 years,1 there has been a considerable advance of knowledge about the cause of diabetes over the past five years.Three interlocking mechanisms have been clearly identified: genetics, viral infections and autoimmunity.2 That genetic influences have a role in the development of . . .