Role for gamma interferon in control of herpes simplex virus type 1 reactivation
Role for gamma interferon in control of herpes simplex virus type 1 reactivation
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DOI：
10.1128/jvi.73.4.3418-3423.1999
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发表时间：
1999-04-01
影响因子：
5.4
通讯作者：
Openshaw, H
中科院分区：
文献类型：
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作者：
Cantin, E;Tanamachi, B;Openshaw, H
在小鼠中，观察慢性炎症细胞和相关的高级伽马干扰素（IFN-gamma）在神经节中产生了小鼠疱疹1型（HSV-1）潜在感染（E，M，M，Cantin，d，r，Hinton，J。Chen）和H. Openshaw，J。Virol，69：4898-4905，1995）促使研究确定IFN-Gamma在维持的作用潜伏期。缺乏IFN-GAMMA（GKO小鼠）或IFN-GAMMA受体（RGKO小鼠）的小鼠与HSV-1接种，并将感染的过程与具有相同遗传背景的IFN-Gamma竞争小鼠（129）（129）进行了比较（129 /sv // ev小鼠）。一项时间课程研究表明，三叉神经节病毒滴度或延迟的时机没有显着差异。在任何小鼠的潜伏期期间，自发性重新激活导致神经节中的传染性病毒均未发生。然而，在将高温应激施加到小鼠中24小时后，在零突变小鼠的多个神经元中检测到HSV-1抗原，但在129/SV // EV控制小鼠中仅单个神经元中检测到HSV-1抗原。单核炎症细胞在这些重新激活的神经元周围紧密聚集，到48小时，卫星细胞也存在免疫染色。通过从神经节中恢复感染性病毒确定的热疗诱导的重新激活的发生率明显高于对照小鼠的发生率：129/sv // eV对照组为11％，在GKO小鼠中为50％（p = 0.0002），50％ RGKO小鼠的33％（p = 0.03）。我们得出的结论是，IFN-gamma不参与重新激活的诱导，而是一旦重新激活HSV。
Observation of chronic inflammatory cells and associated high-level gamma interferon (IFN-gamma) production in ganglia during herpes simplex type 1 (HSV-1) latent infection in mice (E, M, Cantin, D, R, Hinton, J. Chen, and H. Openshaw, J. Virol, 69:4898-4905, 1995) prompted studies to determine a role of IFN-gamma in maintaining latency. Mice lacking IFN-gamma (GKO mice) or the IFN-gamma receptor (RGKO mice) were inoculated with HSV-1, and the course of the infection was compared with that in IFN-gamma-competent mice with the same genetic background (129/Sv//Ev mice). A time course study showed no significant difference in trigeminal ganglionic viral titers or the timing of establishment of latency. Spontaneous reactivation resulting in infectious virus in the ganglion did not occur during latency in any of the mice. However, 24 h after the application of hyperthermic stress to mice, HSV-1 antigens were detected in multiple neurons in the null mutant mice but in only a single neuron in the 129/Sv//Ev control mice. Mononuclear inflammatory cells clustered tightly around these reactivating neurons, and by 48 h, immunostaining was present in satellite cells as well. The incidence of hyperthermia-induced reactivation as determined by recovery of infectious virus from ganglia was significantly higher in the null mutant than in control mice: 11% in 129/Sv//Ev controls, 50% in GKO mice (P = 0.0002), and 33% in RGKO mice (P = 0.03). We concluded that IFN-gamma is not involved in the induction of reactivation but rather contributes to rapid suppression of HSV once it is reactivated.