脑心肌炎（EMC）病毒致糖尿病和非致糖尿病变体在ICR瑞士小鼠中的复制

Replication of diabetogenic and nondiabetogenic variants of encephalomyocarditis (EMC) virus in ICR Swiss mice.

作者信息

Gould C L, Trombley M L, Bigley N J, McMannama K G, Giron D J

出版信息

Proc Soc Exp Biol Med. 1984 Apr;175(4):449-53. doi: 10.3181/00379727-175-41819.

Abstract

The replication of the diabetogenic D (EMC-D) and nondiabetogenic B (EMC-B) variants of encephalomyocarditis virus in various tissues of the murine host was determined. Pancreatic insulin levels were also measured. EMC-D replicated in the spleen, pancreas, heart, lung, and intestines, while EMC-B was limited to the spleen and pancreas. EMC-B interfered with the replication of EMC-D in each of the tissues examined. Insulin levels were initially increased by both viruses. By 4 days postinfection, insulin levels were either normal or undetectable in (EMC-D)-infected animals, but were dramatically elevated in those infected with EMC-B.

摘要

测定了脑心肌炎病毒的致糖尿病D型（EMC-D）和非致糖尿病B型（EMC-B）变体在鼠宿主各种组织中的复制情况。还测量了胰腺胰岛素水平。EMC-D在脾脏、胰腺、心脏、肺和肠道中复制，而EMC-B仅限于脾脏和胰腺。EMC-B在每个检测的组织中都干扰了EMC-D的复制。两种病毒最初都使胰岛素水平升高。感染后4天，感染EMC-D的动物胰岛素水平正常或检测不到，但感染EMC-B的动物胰岛素水平显著升高。