单纯疱疹病毒（HSV）的复制缺陷型突变体可诱导细胞免疫，并能抵御致死性HSV感染。
Replication-defective mutants of herpes simplex virus (HSV) induce cellular immunity and protect against lethal HSV infection.
作者信息
Nguyen L H, Knipe D M, Finberg R W
机构信息
Laboratory of Infectious Diseases, Dana-Farber Cancer Institute, Boston, Massachusetts.
出版信息
J Virol. 1992 Dec;66(12):7067-72. doi: 10.1128/JVI.66.12.7067-7072.1992.
Abstract
Live viruses and live virus vaccines induce cellular immunity more readily than do inactivated viruses or purified proteins, but the mechanism by which this process occurs is unknown. A trivial explanation would relate to the ability of live viruses to spread and infect more cells than can inactivated virus. We have used live but replication-defective mutants to investigate this question. Our studies indicate that the immune responses of mice to live virus differ greatly from the responses to inactivated virus even when the virus does not complete a replicative cycle. Further, these studies indicate that herpes simplex virus-specific T-cell responses can be generated by infection with replication-defective mutant viruses. These data indicate that the magnitude of the cellular immunity to herpes simplex virus may be proportional to the number or quantity of different viral gene products expressed by an immunizing virus.
摘要
活病毒和活病毒疫苗比灭活病毒或纯化蛋白更容易诱导细胞免疫，但这一过程发生的机制尚不清楚。一个简单的解释可能是活病毒比灭活病毒更有能力传播并感染更多细胞。我们使用了活的但复制缺陷型突变体来研究这个问题。我们的研究表明，即使病毒没有完成复制周期，小鼠对活病毒的免疫反应与对灭活病毒的反应也有很大不同。此外，这些研究表明，感染复制缺陷型突变病毒可产生单纯疱疹病毒特异性T细胞反应。这些数据表明，对单纯疱疹病毒的细胞免疫强度可能与免疫病毒表达的不同病毒基因产物的数量或量成正比。
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