Yoon J, Onodera T, Notkins A L
J Gen Virol. 1977 Nov;37(2):225-32. doi: 10.1099/0022-1317-37-2-225.
The diabetogenic capacity of the M-variant of encephalomyocarditis (EMC) virus was markedly diminished after passage in mouse kidney cell cultures. One passage in mice fully restored this capacity. Virus harvested after five passages in either susceptible (SWR/J) or resistant (C57BL/6J) strains of mice was capable of producing diabetes in susceptible SWR/J mice but not in resistant C57BL/6J mice. Resistance was not overcome by inoculating mice with high concentrations of virus. Immunofluorescence studies showed that islets from strains of mice (i.e. CBA, AKR, C57BL/6J, A/J) that did not develop diabetes after infection with EMC virus, nonetheless, contained virus antigens. The percentage of cells in the islets containing virus antigens varied from 3-6% in CBA to 13-5% in A/J. In contrast 38% of the islet cells in susceptible SWR/J mice contained virus antigens. It is concluded that both the genetic background of the host and the passage history of the virus influence the development of diabetes.
脑心肌炎(EMC)病毒M变异体在小鼠肾细胞培养物中传代后,其致糖尿病能力显著降低。在小鼠体内传代一次可完全恢复这种能力。在易感(SWR/J)或抗性(C57BL/6J)小鼠品系中传代五次后收获的病毒,能够使易感的SWR/J小鼠患糖尿病,但不能使抗性的C57BL/6J小鼠患糖尿病。给小鼠接种高浓度病毒并不能克服抗性。免疫荧光研究表明,感染EMC病毒后未患糖尿病的小鼠品系(即CBA、AKR、C57BL/6J、A/J)的胰岛中仍含有病毒抗原。胰岛中含有病毒抗原的细胞百分比在CBA小鼠中为3%-6%,在A/J小鼠中为13%-5%。相比之下,易感的SWR/J小鼠中有38%的胰岛细胞含有病毒抗原。得出的结论是,宿主的遗传背景和病毒的传代历史都会影响糖尿病的发展。