A SEARCH FOR THE PRESENCE OF THE ENTEROVIRAL CAPSID PROTEIN VP-1 IN PANCREASES OF PATIENTS WITH TYPE-1 (INSULIN-DEPENDENT) DIABETES AND PANCREASES AND HEARTS OF INFANTS WHO DIED OF COXSACKIEVIRAL MYOCARDITIS
A SEARCH FOR THE PRESENCE OF THE ENTEROVIRAL CAPSID PROTEIN VP-1 IN PANCREASES OF PATIENTS WITH TYPE-1 (INSULIN-DEPENDENT) DIABETES AND PANCREASES AND HEARTS OF INFANTS WHO DIED OF COXSACKIEVIRAL MYOCARDITIS
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DOI：
10.1007/bf00403323
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发表时间：
1990-05-01
期刊：
影响因子：
8.2
通讯作者：
KANDOLF, R
中科院分区：
文献类型：
--
作者：
FOULIS, AK;FARQUHARSON, MA;KANDOLF, R
Using an antiserum raised to a recombinant coxsackie virus B3 capsid protein, VP1, an immunocytochemical technique was developed which was capable of detecting the presence of all coxsackie B viruses in formalin fixed paraffin embedded infected tissue culture cells. This technique was tested on autopsy heart and pancreas from 21 patients who were thought to have died of acute coxsackie virus B myocarditis. Cardiac myocytes were positive for the VP1 protein in 12 of 20 cases where the heart was available for study. Insulitis was present in the pancreas in seven of these cases and in all seven islet endocrine cells containing VP1 were found. VP1 was only rarely found in exocrine pancreas. In heart and pancreas, cells shown to contain VP1 usually showed signs of necrosis. Autopsy pancreases from 88 patients who had died at clinical presentation of Type 1 (insulin-dependent) diabetes mellitus showed no evidence of the presence of VP1. The continuing destruction of insulin-secreting B cells seen at the time of death in the diabetic pancreas is unlikely to be due t a direct cytopathic effect of a coxsackie B virus. However, this study does not exclude the possibility that a persistent infection of B cells by a defective enterovirus may result in their destruction by an autoimmune mechanism.
