CYTOKINE INVOLVEMENT IN VIRAL PERMISSIVENESS AND THE PROGRESSION OF HIV DISEASE

被引:20
作者
BUTERA, ST
机构
关键词
PERMISSIVENESS; HIV-1; TUMOR NECROSIS FACTOR; VIRAL ACTIVATION;
D O I
10.1002/jcb.240530411
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Many viruses have evolved novel means of exploiting host defense mechanisms for their own survival. This exploitation may be best exemplified by the interrelationships between certain viruses and the host cytokine networks. Many viruses, including the human immunodeficiency virus type-1 (HIV-1), rely on the liberation and cellular action of host immune cytokines to expand their host cell range, to regulate their cellular expression, and to maintain their dormant state until the proper extracellular conditions arise. As again exemplified by HIV-1, viruses may also take an active role regulating cytokine expression and cell surface cytokine receptors. Because the viral life cycle, and in particular the HIV-1 life cycle, is so intertwined with cytokine regulatory networks, these networks represent potential points for therapeutic intervention. As our understanding of cellular cytokine pathways involved in viral infection and replication continues to expand, so too will our ability to design rational anti-viral therapies to alter multiple steps along the viral life cycle. (C) 1993 Wiley-Liss, Inc.*
引用
收藏
页码:336 / 342
页数:7
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