Suckling A J, Jagelman S, Webb H E
Infect Immun. 1977 Feb;15(2):386-91. doi: 10.1128/iai.15.2.386-391.1977.
Mice infected with an avirulent strain of Semliki forest virus show an increase in the activity of some of the brain lysosomal glycosidases. The increase in activity of these enzymes has been correlated with the histological, virological, and serological changes that result from the infection in the presence and absence of immunosuppression. Semliki forest virus alone caused the development of a mild encephalitis with perivascular infiltration, microgliosis, astrocyte hypertrophy, and a focal spongiform encephalopathy, together with an increased activity of brain N-acetyl-beta-D-glucosaminidase and beta-glucuronidase. Antilymphocyte serum given after infection marginally affected the course of the disease. Cyclophosphamide markedly delayed the development of the spongy changes in the increase in enzyme activities, but not the perivascular infiltration. It is suggested that the increased activity of the lysosomal glycosidases studied may be linked both to the development of a successful immune response and to the focal spongiform changes produced by the infection.
感染了减毒株辛德毕斯病毒的小鼠,其大脑中某些溶酶体糖苷酶的活性会增加。这些酶活性的增加与在有或没有免疫抑制情况下感染所导致的组织学、病毒学和血清学变化相关。单独的辛德毕斯病毒会引发轻度脑炎,伴有血管周围浸润、小胶质细胞增生、星形胶质细胞肥大和局灶性海绵状脑病,同时大脑N-乙酰-β-D-氨基葡萄糖苷酶和β-葡萄糖醛酸酶的活性增加。感染后给予抗淋巴细胞血清对疾病进程影响甚微。环磷酰胺显著延迟了海绵状变化的发展以及酶活性的增加,但并未延迟血管周围浸润。研究表明,所研究的溶酶体糖苷酶活性增加可能与成功的免疫反应发展以及感染所产生的局灶性海绵状变化均有关联。