Butera S T
Retrovirus Diseases Branch, Centers for Disease Control and Prevention, Atlanta, Georgia 30333.
J Cell Biochem. 1993 Dec;53(4):336-42. doi: 10.1002/jcb.240530411.
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.
许多病毒已经进化出利用宿主防御机制来实现自身生存的新手段。这种利用在某些病毒与宿主细胞因子网络之间的相互关系中体现得最为明显。许多病毒，包括1型人类免疫缺陷病毒（HIV-1），依赖宿主免疫细胞因子的释放及其细胞作用来扩大宿主细胞范围、调节细胞表达，并维持其休眠状态，直至合适的细胞外条件出现。同样以HIV-1为例，病毒也可能在调节细胞因子表达和细胞表面细胞因子受体方面发挥积极作用。由于病毒生命周期，尤其是HIV-1的生命周期，与细胞因子调节网络紧密相连，这些网络代表了治疗干预的潜在靶点。随着我们对参与病毒感染和复制的细胞因子途径的理解不断深入，我们设计合理的抗病毒疗法以改变病毒生命周期多个步骤的能力也将不断提高。
