Key result
Coxsackievirus B4 infection in mice resulted in significant cellular alterations in the pancreas in 32 of 56 (57.1%) cases, ranging from focal degeneration to widespread necrosis and inflammation.
Coxsackievirus B4 infection in mice causes significant pathologic changes in the pancreas, suggesting a potential viral etiology for subclinical and overt diabetes mellitus in humans.
No clinical implications; hypothesis-generating for viral triggers of human diabetes.
Pathologic changes in the exocrine and endocrine portions of the pancreas were observed in suckling and young adult mice infected with coxsackievirus B4. Thirty-two of 56 infected mice studied histologically showed significant cellular alterations. Generally, the changes ranged from focal and mild degeneration to widespread necrosis and inflammation. Electron micrographs of other infected mice showed derangement of the endoplasmic reticulum in acinar cells and various degrees of degranulation and cellular disruption in the islets. It seems likely that viruses may produce similar damage to the pancreas in man, and it is postulated that viral pancreatitis may cause subclinical diabetes as well as overt diabetes mellitus of varying degrees. For some time we have been interested in the pathologic changes in a variety of organs of animals infected with the coxsackievirus B4. Our attention has been primarily directed toward the myocardium and associated structures, ie, endocardium and valves,1-6and to
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George E. Burch (1971) studied Coxsackievirus B4 infection (n=56). Coxsackievirus B4 infection was evaluated on Significant cellular alterations in the pancreas. Coxsackievirus B4 infection in mice resulted in significant cellular alterations in the pancreas in 32 of 56 (57.1%) cases, ranging from focal degeneration to widespread necrosis and inflammation.
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