Chairez R, Yoon J W, Notkins A L
Virology. 1978 Apr;85(2):606-11. doi: 10.1016/0042-6822(78)90465-8.
Monolayers of pancreatic β-cells from strains of mice susceptible (SJL/J) and resistant (C57BL/6J) to the development of virus-induced diabetes mellitus were inoculated with the M variant of encephalomyocarditis (EMC) virus. Immunofluorescence showed that viral antigens appeared in up to 10 times more β cells from susceptible SJL/J mice than from resistant C57BL/6J mice. Infectious center assays revealed that 10–30 times more SJL/J β cells contained infectious virus than C57BL/6J β cells. Viral attachment experiments showed no difference in the binding of EMC virus when embryonic fibroblasts, pancreatic fibroblasts, and kidney cells from SJL/J and C57BL/6J mice were compared. However, at least twice as much virus attached to the pancreatic β cells from susceptible than from resistant strains of mice. Our data suggest that genetically determined differences in viral receptors on the surface of β cells may be one of the factors controlling susceptibility to EMC-induced diabetes mellitus.
用脑心肌炎(EMC)病毒的M变种接种对病毒诱导的糖尿病敏感(SJL/J)和抗性(C57BL/6J)的小鼠品系的胰腺β细胞单层。免疫荧光显示,与抗性C57BL/6J小鼠相比,易感SJL/J小鼠的β细胞中出现病毒抗原的数量多达10倍。感染中心测定显示,含有感染性病毒的SJL/Jβ细胞比C57BL/6Jβ细胞多10 - 30倍。病毒附着实验表明,当比较SJL/J和C57BL/6J小鼠的胚胎成纤维细胞、胰腺成纤维细胞和肾细胞时,EMC病毒的结合没有差异。然而,附着在易感小鼠品系胰腺β细胞上的病毒至少是抗性品系的两倍。我们的数据表明,β细胞表面病毒受体的遗传决定差异可能是控制对EMC诱导的糖尿病易感性的因素之一。