Division of Virology, Department of Pathology, University of Cambridge, Cambridge, United Kingdom.
PLoS One. 2007 Aug 8;2(8):e705. doi: 10.1371/journal.pone.0000705.
Herpesviruses maintain long-term infectivity without marked antigenic variation. They must therefore evade neutralization by other means. Immune sera block murine gammaherpesvirus-68 (MHV-68) infection of fibroblasts, but fail to block and even enhance its infection of IgG Fc receptor-bearing cells, suggesting that the antibody response to infection is actually poor at ablating virion infectivity completely. Here we analyzed this effect further by quantitating the glycoprotein-specific antibody response of MHV-68 carrier mice. Gp150 was much the commonest glycoprotein target and played a predominant role in driving Fc receptor-dependent infection: when gp150-specific antibodies were boosted, Fc receptor-dependent infection increased; and when gp150-specific antibodies were removed, Fc receptor-dependent infection was largely lost. Neither gp150-specific monoclonal antibodies nor gp150-specific polyclonal sera gave significant virion neutralization. Gp150 therefore acts as an immunogenic decoy, distorting the MHV-68-specific antibody response to promote Fc receptor-dependent infection and so compromise virion neutralization. This immune evasion mechanism may be common to many non-essential herpesvirus glycoproteins.
疱疹病毒在没有明显抗原变异的情况下保持长期感染性。因此，它们必须通过其他方式逃避中和作用。免疫血清可阻断小鼠γ疱疹病毒-68（MHV-68）对成纤维细胞的感染，但不能阻断甚至增强其对 IgG Fc 受体细胞的感染，这表明感染后的抗体反应实际上很难完全消除病毒粒子的感染力。在这里，我们通过定量分析 MHV-68 携带者小鼠的糖蛋白特异性抗体反应进一步分析了这种效应。gp150 是最常见的糖蛋白靶标，在驱动 Fc 受体依赖性感染中起主要作用：当 gp150 特异性抗体被增强时，Fc 受体依赖性感染增加；当 gp150 特异性抗体被去除时，Fc 受体依赖性感染基本上消失。gp150 特异性单克隆抗体和 gp150 特异性多克隆血清均不能显著中和病毒粒子。因此，gp150 充当免疫诱饵，改变 MHV-68 特异性抗体反应以促进 Fc 受体依赖性感染，从而损害病毒粒子中和作用。这种免疫逃避机制可能在许多非必需的疱疹病毒糖蛋白中都很常见。
