DETECTION OF VARICELLA-ZOSTER VIRUS-SPECIFIC DNA-SEQUENCES IN CEREBROSPINAL-FLUID FROM PATIENTS WITH ACUTE ASEPTIC-MENINGITIS AND NO CUTANEOUS LESIONS
DETECTION OF VARICELLA-ZOSTER VIRUS-SPECIFIC DNA-SEQUENCES IN CEREBROSPINAL-FLUID FROM PATIENTS WITH ACUTE ASEPTIC-MENINGITIS AND NO CUTANEOUS LESIONS
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DOI：
10.1002/jmv.1890430403
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发表时间：
1994-08-01
影响因子：
12.7
通讯作者：
MARTINEZMARTIN, P
中科院分区：
文献类型：
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作者：
ECHEVARRIA, JM;CASAS, I;MARTINEZMARTIN, P
急性无菌性脑膜炎（AAM）是水痘-带状疱疹病毒（VZV）复发后的一种罕见表现，通常被认为是细胞免疫功能受损患者皮肤感染的并发症。然而，间接证据表明，VZV相关的AAM也可能对病毒从支持潜伏期的细胞直接传播到软脑膜作出反应。聚合酶链反应（PCR）被用来扩增VZV特异性DNA序列的系列脑脊液（CSF）样本从21例AAM，谁提出的实验室证据的鞘内生产VZV特异性抗体的后续行动。其中11例患者从未出现皮肤带状疱疹样病变。在所有患者的CSF中检测到VZV-DNA序列，皮肤测试仪，以及从6例（55%）没有皮肤病变。在脑脊液中特异性抗体升高之前，6例患者中存在病毒DNA序列，7例阳性患者在随访期间消失。这些结果支持VZV参与正常年轻人中AAM的病因学，并强烈表明病毒可以直接到达并从潜伏感染的脊神经节感染CNS。(C)1994 Wiley-Liss，Inc.
Acute aseptic meningitis (AAM) is considered as an uncommon manifestation of varicella-zoster virus (VZV) recrudescence and is usually regarded as a complication of the cutaneous infection in patients with impaired cellular immunity. Indirect evidence suggests, however, that VZV-associated AAM may also respond to direct spread of the virus to the leptomeninges from the cells supporting the latency. The polymerase chain reaction (PCR) was used to amplify VZV-specific DNA sequences in serial cerebrospinal fluid (CSF) samples from 21 patients with AAM, who presented laboratory evidence of intrathecal production of VZV-specific antibody on follow-up. Eleven of these patients never showed cutaneous zosteriform lesions. VZV-DNA sequences were detected in the CSF from all patients with cutaneous tester, as well as from six patients (55%) lacking skin lesions. Viral DNA sequences were present in six cases before the rise in specific antibody was seen in CSF, disappearing during follow-up in the seven positive cases. These results support the proposed involvement of VZV in the etiology of AAM seen among normal young adults and strongly suggest that the virus can reach directly and infect the CNS from the latently infected spinal ganglia. (C) 1994 Wiley-Liss, Inc.