THE MOLECULAR-BASIS OF HERPES-SIMPLEX VIRUS PATHOGENICITY

被引:12
作者
FAWL, RL
ROIZMAN, B
机构
[1] Marjorie B. Kovler Viral Oncology Laboratories, The University of Chicago, Chicago, IL 60637
来源
SEMINARS IN VIROLOGY | 1994年 / 5卷 / 04期
关键词
HERPES SIMPLEX VIRUS; NEUROVIRULENCE; NEUROINVASIVENESS; NEUROGROWTH; LATENCY; REACTIVATION;
D O I
10.1006/smvy.1994.1029
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
The key features of herpes simplex viruses are cell destruction with considerable pathology, particularly in productive infections of the central nervous system, and ability to remain latent in sensory and autonomic neurons of the peripheral nervous system. In cells in culture, approximately half of the 74 known different genes of the virus are not essential for viral replication. For the most part, these genes are required for efficient viral replication in experimental animal models. Mutations in a small number of viral genes have been shown to decrease the ability of the virus to access the central nervous system or in ability to multiply efficiently. These genes play a key role in defining the pathogenic properties of the virus. Current evidence suggests that viral gene expression is not required for initiation and maintenance of the latent state. Latency reflects the capacity of the cell to specifically and transiently repress viral gene expression.
引用
收藏
页码:261 / 271
页数:11
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