Horvath Curt M
Immunobiology Center, The Mount Sinai School of Medicine, One Gustave L. Levy Place, Box 1630, New York, NY 10029, USA.
Cytokine Growth Factor Rev. 2004 Apr-Jun;15(2-3):117-27. doi: 10.1016/j.cytogfr.2004.02.003.
The signal transducer and activator of transcription (STAT) family proteins are essential mediators of cytokine and growth factor functions. The interferon (IFN) family of cytokines is well known as modulators of both innate and adaptive anti-microbial immunity. In response to the evolutionary struggle between host and pathogen, many viruses have developed strategies to bypass the IFN antiviral system. Uniquely, the paramyxoviruses have developed the ability to efficiently inactivate STAT protein function, in many cases using a single virus-encoded protein called 'V'. The V protein plays a central role in STAT inhibition, but mechanistic studies have revealed great diversity in V-dependent STAT signaling evasion among paramyxovirus species. These examples of IFN evasion by STAT protein inactivation can help define targets for antiviral drug design or improving vaccine regimens. Moreover, understanding these STAT inhibition mechanisms are likely to reveal strategic options for the design of STAT-directed therapeutics for treatment of diseases characterized by cytokine hyperactivity.
信号转导与转录激活因子（STAT）家族蛋白是细胞因子和生长因子功能的重要介质。细胞因子中的干扰素（IFN）家族作为先天性和适应性抗微生物免疫的调节剂而广为人知。为应对宿主与病原体之间的进化斗争，许多病毒已开发出绕过IFN抗病毒系统的策略。独特的是，副粘病毒已发展出有效灭活STAT蛋白功能的能力，在许多情况下使用一种名为“V”的单一病毒编码蛋白。V蛋白在STAT抑制中起核心作用，但机制研究表明，副粘病毒物种之间依赖V的STAT信号逃避存在很大差异。这些通过STAT蛋白失活逃避IFN的例子有助于确定抗病毒药物设计或改进疫苗方案的靶点。此外，了解这些STAT抑制机制可能会揭示设计针对细胞因子活性过高所特征疾病的STAT导向疗法的战略选择。
