Molecular mechanism of persistent infection of SSPE virus

SSPE病毒持续感染的分子机制

• 批准号: 10470047
• 负责人: ABE Satoshi
• 金额: $ 4.03万
• 依托单位: Niigata University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (B)
• 财政年份: 1998
• 资助国家: 日本
• 起止时间: 1998 至 2000
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-10470047/
• 关键词: Subacutescrelosing panencephalitis; SSPE; Persistent infection; Gene mutation

Subacute sclerosing panericephalitis (SSPE) is a chronic progressive disease of the central nervous system caused by a persistent infection of a variant of measles virus (SSPE virus). In this study, RT-PCR and CDNA cloning were used to examine the structural protein genes of SSPE virus in the brain and lymph node from a case ofSSPE. Six major structural protein genes (NP, P, M, F, HA and L) were detected in both brain and lymph node in our case. In the examination of the brain, multiple independent clones of the entire length of the coding region of the genes were sequenced.The identical multiple mutations were revealed in the genes in comparison with Edmonston strain of measles virus. The lymph node clones had identical mutations with brain clones and had multiple additional mutations, indicating that the viral genes were still under the influence of the hypermutation mechanism. These findings suggest mat in addition to the central nervous system, the lymph node may also have a role in the progression of SSPE. Ninety-three percent of these mutations was transition (U to C). This biased hypermutation was considered to be specific for SSPE virus.Translocations or chromosomal aberrations were not found in our case. Differentially expressed unique genes were not detected in the brain and lymph node by CDNA subtraction methods.

亚急性硬化性麻疹（SSPE）是一种慢性进行性中枢神经系统疾病，由麻疹病毒（SSPE病毒）的一种变异体持续感染引起。本研究采用RT-PCR和cDNA克隆技术对1例SSPE患者脑组织和淋巴结中SSPE病毒的结构蛋白基因进行了检测。在我们的病例中，在脑和淋巴结中都检测到六种主要的结构蛋白基因（NP，P，M，F，HA和L）。在脑组织检查中，对多个独立克隆的基因编码区全长进行了测序，并与麻疹病毒Edmonston株进行了比较，发现其基因存在相同的多处突变。淋巴结克隆与脑克隆有相同的突变，并有多个额外的突变，表明病毒基因仍在超突变机制的影响下。这些发现表明，除了中枢神经系统，淋巴结也可能在SSPE的进展中发挥作用。这些突变中有93%是转换（U到C）。我们的病例中未发现易位或染色体畸变。用cDNA差减法在脑和淋巴结中未检测到差异表达的独特基因。

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