Kisaki Hisanobu, Hato Naohito, Mizobuchi Mutsuhiko, Honda Nobumitsu, Takahashi Hirotaka, Wakisaka Hiroyuki, Hitsumoto Yasuo, Yanagihara Naoaki, Gyo Kiyofumi
Department of Otolaryngology, Ehime University School of Medicine, Onsen-gun, Ehime, Japan.
Acta Otolaryngol. 2005 Mar;125(3):316-21. doi: 10.1080/00016480410023083.
Although both T-cell subsets are essential for inhibiting HSV-1 reactivation in the GG, CD4 + T cells play a more important role in host defense against virus replication.
To elucidate the host immunological factors that participate in herpes simplex virus type 1 (HSV-1) reactivation in the geniculate ganglia (GG) and lead to facial paralysis, we developed a mouse model of facial paralysis that involved the reactivation of HSV-1 following general immune suppression.
Eight weeks after recovery from primary facial paralysis caused by inoculating the auricle with HSV-1 the auricle was scratched and mice (n = 69) were given an i.p. injection of either anti-CD4 (n = 46) or anti-CD8 (n = 23) monoclonal antibody to deplete specific T-lymphocyte subsets. Following this reactivation procedure, the rate of recurrent facial paralysis was compared between the two models. The GG were examined histopathologically and using polymerase chain reaction to detect HSV-1 DNA.
Facial paralysis developed in 42% of mice in the anti-CD4 model and in 13% in the anti-CD8 model. HSV-1 DNA was detected in 50% of the mice in both models. Histopathologically, neurons were destroyed in parts of the GG and numerous virus particles were seen in the surviving neurons.
虽然两种T细胞亚群对于抑制膝状神经节中的单纯疱疹病毒1型（HSV-1）再激活都是必不可少的，但CD4 + T细胞在宿主抵抗病毒复制的防御中发挥着更重要的作用。
为了阐明参与膝状神经节（GG）中单纯疱疹病毒1型（HSV-1）再激活并导致面瘫的宿主免疫因素，我们建立了一种面瘫小鼠模型，该模型涉及在全身免疫抑制后HSV-1的再激活。
在用HSV-1接种耳廓引起原发性面瘫恢复8周后，刮擦耳廓，并给小鼠（n = 69）腹腔注射抗CD4（n = 46）或抗CD8（n = 23）单克隆抗体以耗尽特定的T淋巴细胞亚群。在这个再激活过程之后，比较两个模型之间复发性面瘫的发生率。对膝状神经节进行组织病理学检查，并使用聚合酶链反应检测HSV-1 DNA。
抗CD4模型中42%的小鼠发生了面瘫，抗CD8模型中13%的小鼠发生了面瘫。在两个模型中，50%的小鼠检测到HSV-1 DNA。组织病理学检查显示，膝状神经节的部分神经元被破坏，在存活的神经元中可见大量病毒颗粒。
