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首页> 美国卫生研究院文献>The Journal of Experimental Medicine >In Vivo Role of Complement-Interacting Domains of Herpes Simplex Virus Type 1 Glycoprotein Gc
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In Vivo Role of Complement-Interacting Domains of Herpes Simplex Virus Type 1 Glycoprotein Gc

机译：单纯疱疹病毒1型糖蛋白Gc的互补相互作用域的体内作用。

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摘要

Immune evasion is critical for survival of viruses that establish persistent or recurrent infections. However, at the molecular level, little is known about how viruses evade immune attack in vivo. Herpes simplex virus (HSV)-1 glycoprotein gC has two domains that are involved in modulating complement activation; one binds C3, and the other is required for blocking C5 and properdin (P) binding to C3. To evaluate the importance of these regions in vivo, HSV-1 gC mutant viruses were constructed that lacked one or both gC domains and studied in a murine model of infection. Each gC region of complement regulation contributed to virulence; however, the C3 binding domain was far more important, as virus lacking this domain was much less virulent than virus lacking the C5/P inhibitory domain and was as attenuated as virus lacking both domains. Studies in C3 knockout mice and mice reconstituted with C3 confirmed that the gC domains are inhibitors of complement activation, accounting for a 50-fold difference in virulence between mutant and wild-type viruses. We conclude that the C3 binding domain on gC is a major contributor to immune evasion and that this site explains at a molecular level why wild-type virus resists complement attack.
机译：逃避免疫对于建立持续性或复发性感染的病毒的生存至关重要。但是，在分子水平上，对于病毒如何逃避体内免疫攻击知之甚少。单纯疱疹病毒（HSV）-1糖蛋白gC具有两个域，参与调节补体激活。一个与C3结合，另一个对于阻断C5和备解素（P）与C3的结合是必需的。为了评估体内这些区域的重要性，构建了缺少一个或两个gC结构域的HSV-1 gC突变病毒，并在小鼠感染模型中进行了研究。补体调节的每个gC区域均导致了毒力；但是，C3结合域更为重要，因为缺少该域的病毒的毒性要比缺少C5 / P抑制域的病毒弱得多，并且与缺少两个域的病毒一样弱。对C3基因敲除小鼠和C3重组小鼠的研究证实，gC结构域是补体激活的抑制剂，这说明突变型病毒和野生型病毒之间的毒力差异为50倍。我们得出的结论是，gC上的C3结合域是免疫逃逸的主要因素，并且该位点在分子水平上解释了为何野生型病毒抵抗补体攻击。

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