Variable patterns of varicella-zoster virus reactivation in Ramsay Hunt syndrome
Variable patterns of varicella-zoster virus reactivation in Ramsay Hunt syndrome
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DOI：
10.1002/jmv.20181
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发表时间：
2004-10-01
影响因子：
12.7
通讯作者：
Fukuda, S
中科院分区：
文献类型：
--
作者：
Aizawa, H;Ohtani, F;Fukuda, S
水痘-带状疱疹病毒（VZV）激活导致Ramsay Hunt综合征面瘫的机制尚不清楚。本文分析了42例Ramsay Hunt综合征患者VZV负荷与面瘫发生的关系。根据带状疱疹和面瘫出现的时间分为3组：Ⅰ组（带状疱疹先行组，n = 13），Ⅱ组（带状疱疹同时出现组，n = 22），Ⅲ组（面瘫先行组，n = 7）。采用实时荧光定量PCR方法检测唾液中VZV DNA拷贝数，并检测配对血清中抗VZV IgG和IgM抗体。在第一组中，VZV DNA阳性率较低，病毒载量在首次住院后逐渐下降。在大多数情况下，抗VZV抗体水平当时已经增加。在组III中，病毒载量在瘫痪发作后趋于增加，并在带状疱疹出现时达到峰值。抗VZV抗体的水平在瘫痪发作时很低，但配对血清进行测试时显示出显着增加。在第II组中，病毒载量和抗VZV抗体水平的变化与第I组或第III组的行为相似。这些结果表明，在拉姆齐亨特综合征的面瘫可以发生在不同的时间之间的早期和回归阶段的VZV再激活，这表明有可变的发展模式的面神经功能障碍引起的VZV再激活和神经炎的进展。
The mechanism by which reactivation of varicella-zoster virus (VZV) causes facial paralysis in Ramsay Hunt syndrome remains unclear. The relationship between VZV load and the onset of facial paralysis was analyzed in 42 patients with Ramsay Hunt syndrome. The patients were divided into three groups according to the times of appearance of zoster and of facial paralysis; group I (zoster preceding, n = 13), group II (simultaneous, n = 22), group III (paralysis preceding, n = 7). A real-time quantitative PCR assay was used to measure VZV DNA copy number in saliva, and paired sera were assayed for anti-VZV IgG and IgM antibodies. In group I, the VZV DNA-positive rate was low and virus load decreased gradually after the initial hospital visit around the time of onset of paralysis. The level of anti-VZV antibodies had in most cases already increased at that time. In group III, viral load tended to increase after the onset of paralysis and peaked around the time of appearance of zoster. The level of anti-VZV antibodies was low at the onset of paralysis but showed a significant increase when paired sera were tested. In group II, virus load and changes in level of anti-VZV antibodies either resembled group I or group III behavior. These results indicate that facial paralysis in Ramsay Hunt syndrome can occur at various times between the early and the regression phase of VZV reactivation, suggesting that there are variable patterns of development of facial nerve dysfunction caused by VZV reactivation and the progression of neuritis.