Lubinski J, Nagashunmugam T, Friedman H M
Department of Medicine, University of Pennsylvania School of Medicine, 536 Johnson Pavilion, Philadelphia, PA, 19104-6073, USA.
Semin Cell Dev Biol. 1998 Jun;9(3):329-37. doi: 10.1006/scdb.1998.0242.
Viruses have evolved strategies to evade immunity mediated by antibody and complement. Herpesviruses and coronaviruses encode IgG Fc binding proteins that inhibit IgG activity, enabling the virus or infected cell to escape antibody attack. Herpesviruses, vaccinia virus and HIV-1 have the capacity to interfere with complement, either by incorporation of cellular complement regulatory proteins into the virion envelope or cell membrane, or by expression of viral molecules that mimic functions of complement regulatory proteins. The structure and biological activities of herpes simplex virus type 1 (HSV-1) glycoproteins gE, gI and gC are described. These glycoproteins protect HSV from immune attack; HSV-1 gE/gI form a complex that binds the Fc domain of IgG while gC is a C3b binding complement regulatory protein, providing a survival advantage to the virus in vitro and in vivo by inhibiting immune functions.
病毒已经进化出逃避由抗体和补体介导的免疫的策略。疱疹病毒和冠状病毒编码抑制IgG活性的IgG Fc结合蛋白,使病毒或受感染细胞能够逃避抗体攻击。疱疹病毒、痘苗病毒和HIV-1有干扰补体的能力,要么通过将细胞补体调节蛋白整合到病毒粒子包膜或细胞膜中,要么通过表达模拟补体调节蛋白功能的病毒分子。描述了单纯疱疹病毒1型(HSV-1)糖蛋白gE、gI和gC的结构及生物学活性。这些糖蛋白保护HSV免受免疫攻击;HSV-1 gE/gI形成一个结合IgG Fc结构域的复合物,而gC是一种C3b结合补体调节蛋白,通过抑制免疫功能在体外和体内为病毒提供生存优势。