Szopa T M, Ward T, Dronfield D M, Portwood N D, Taylor K W
Department of Biochemistry, London Hospital Medical College, UK.
Diabetologia. 1990 Jun;33(6):325-8. doi: 10.1007/BF00404634.
Infections with Coxsackie viruses (especially Coxsackie B4) are thought to be involved in the pathogenesis of diabetes. Many interdependent variables determine the outcome of an infection with a Coxsackie virus, one of them being the tropism of the virus for a specific tissue. The extent to which Beta cell tropic variants of Coxsackie B4 virus occur naturally was assessed. Human isolates of this virus were tested in an in vitro system in which elevated insulin release from infected islets incubated at a non-stimulatory (2 mmol/l) glucose concentration appears to be related to viral attack. Using this technique, 8/24 isolates tested, impaired secretory function in mouse islets. Some strains of Coxsackie B4 virus, therefore, will directly infect mouse islets in vitro leading to changes in islet cell function. In conclusion, these findings confirm that variants of Coxsackie B4 virus with the potential to damage Beta cells occur quite frequently in the natural population. In certain circumstances the damage they inflict on Beta cells may cause destruction of these cells, or precipitate overt diabetes.
柯萨奇病毒(尤其是柯萨奇B4病毒)感染被认为与糖尿病的发病机制有关。许多相互依存的变量决定了柯萨奇病毒感染的结果,其中之一是病毒对特定组织的嗜性。评估了柯萨奇B4病毒β细胞嗜性变体自然发生的程度。该病毒的人类分离株在体外系统中进行测试,在该系统中,在非刺激(2 mmol/l)葡萄糖浓度下孵育的受感染胰岛中胰岛素释放增加似乎与病毒攻击有关。使用该技术,24株测试分离株中有8株损害了小鼠胰岛的分泌功能。因此,一些柯萨奇B4病毒株在体外会直接感染小鼠胰岛,导致胰岛细胞功能发生变化。总之,这些发现证实,在自然人群中,具有损害β细胞潜力的柯萨奇B4病毒变体相当常见。在某些情况下,它们对β细胞造成的损害可能会导致这些细胞的破坏,或引发显性糖尿病。