Post-exposure vaccination improves gammaherpesvirus neutralization.

Post-exposure vaccination improves gammaherpesvirus neutralization.
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DOI:
10.1371/journal.pone.0000899
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发表时间:
2007-09-19
期刊:
影响因子:
3.7
通讯作者:
Stevenson PG
Stevenson PG
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Gillet L;May JS;Stevenson PG

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尽管产生了病毒特异性抗体,疱疹病毒携带者仍会传播感染。因此,它们的抗体应答不一定是最佳的。感染控制的一个重要问题是接种带菌者是否可以提高病毒中和作用。对鼠γ-疱疹病毒-68(MHV-68)的抗体应答阻断细胞结合,但不能阻断甚至增强骨髓细胞的IgG Fc受体依赖性感染。因此,病毒膜融合保持完整。尽管gH/gL特异性单克隆抗体可以在接近膜融合的结合后步骤阻断感染,但gH/gL在病毒载体中是相对次要的抗体靶标。我们在这里表明,gH/gL特异性抗体可以阻断Fc受体独立和Fc受体依赖性感染,并与gH/gL融合蛋白的疫苗接种病毒载体提高其在体外和体内的病毒中和能力。这种方法有可能减少疱疹病毒的传播。
Herpesvirus carriers transmit infection despite making virus-specific antibodies. Thus, their antibody responses are not necessarily optimal. An important question for infection control is whether vaccinating carriers might improve virus neutralization. The antibody response to murine gamma-herpesvirus-68 (MHV-68) blocks cell binding, but fails to block and even enhances an IgG Fc receptor-dependent infection of myeloid cells. Viral membrane fusion therefore remains intact. Although gH/gL-specific monoclonal antibodies can block infection at a post-binding step close to membrane fusion, gH/gL is a relatively minor antibody target in virus carriers. We show here that gH/gL-specific antibodies can block both Fc receptor-independent and Fc receptor-dependent infections, and that vaccinating virus carriers with a gH/gL fusion protein improves their capacity for virus neutralization both in vitro and in vivo. This approach has the potential to reduce herpesvirus transmission.
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