角膜复制是单纯疱疹病毒 1 在缺乏病毒宿主关闭的情况下毒力的干扰素反应非依赖性瓶颈。
Corneal replication is an interferon response-independent bottleneck for virulence of herpes simplex virus 1 in the absence of virion host shutoff.
机构信息
Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, MO, USA.
出版信息
J Virol. 2012 Jul;86(14):7692-5. doi: 10.1128/JVI.00761-12. Epub 2012 May 2.
Abstract
Herpes simplex viruses lacking the virion host shutoff function (Δvhs) are avirulent and hypersensitive to type I and type II interferon (IFN). In this study, we demonstrate that even in the absence of IFN responses in AG129 (IFN-αβγR(-/-)) mice, Δvhs remains highly attenuated via corneal infection but is fully virulent via intracranial infection. The data demonstrate that the interferon-independent inherent replication defect of Δvhs has a significant impact upon peripheral replication and neuroinvasion.
摘要
单纯疱疹病毒缺失病毒宿主关闭功能（Δvhs）后会失去毒力，并对 I 型和 II 型干扰素（IFN）变得高度敏感。在这项研究中，我们证明了，即使在缺乏 IFN 反应的 AG129（IFN-αβγR(-/-)) 小鼠中，通过角膜感染，Δvhs 仍然高度减毒，但通过颅内感染则完全具有毒力。这些数据表明，Δvhs 的干扰素非依赖性固有复制缺陷对周围复制和神经侵袭有重大影响。
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