@article{oai:az.repo.nii.ac.jp:00005149, author = {西野, 佳以 and 斑目, 広郎 and 舟場, 正幸 and Nishino, Yoshii and Madarame, Hiroo and Funaba, Masayuki}, journal = {麻布大学雑誌, Journal of Azabu University}, month = {Mar}, note = {ボルナ病ウイルス(borna disease virus;BDV)は,馬や羊に髄膜炎あるいは脳脊髄炎をおこし,神経疾患や時に致死的な経過を引き起こすボルナ病の原因ウイルスである。ところが,ラットにおいて高病原性であるCRNP5株は,免疫応答の未熟な新生仔ラットに感染させると脳炎は認められないものの重篤なボルナ病を発症する。従って,CRNP5株は免疫応答非依存的に感染ラットを発症させること,すなわち直接的/間接的な中枢神経障害がある可能性が示唆されていた。そこで,本研究では,ボルナ病発症における宿主の免疫応答の必要性について調べるために,T細胞機能欠如ラット(ヌードラット)における病原性を解析した。4週令のヌードラットにCRNP5株とCRP3株を感染したところ,CRNP5株感染群は全頭重篤なボルナ病を発症したが,CRP3株感染ラットは7週間の観察期間中に発症は認められなかった。CRNP5株感染ラットでは,海馬の神経細胞層が消失し,特に錐体細胞層における神経細胞変性が顕著だった。以上の結果から,CRP3株はT細胞性免疫応答介在性にボルナ病を発症すること,一方,CRNP5株は発症には宿主のT細胞性免疫は必要としていないことが強く示唆された。, Borna disease virus (BDV) causes classical Borna disease (BD), a fatal mononuclear inflammatory encephalomyelitis with severe signs of neurological disease in horses and sheep. Classical BD in adult rats is in large part due to immunopathogenic damage to the nervous system by blood-borne inflammatory cells. However, newborn rats inoculated with mouse-adapted BDV variant (CRNP5) develop severe neurological disease without encephalitis. Thus, it is suggested that rats infected with CRNP5 develop BD without immune response, and CRNP5 is directly and/or indirectly due to damage to the central nervous system. In order to gain a better understanding of immune responses contributions to BD outcomes, we studied the neuropathogenesis of BDV in athymic nude rats (rnu/rnu), naturally deficient in the T-lymphocyte system. Four-week old female nude rats were either inoculated intracranially with 2×10^3 FFU of rat-adapted prototype variant (CRP3) (n=7) or CRNP5 (n=7) or an equal volume of uninfected mouse brain material (n=7). All CRNP5-infected nude rats developed fatal neurological disease although all CRP3-infected rats survived to 7 week post inoculation without obvious neurological signs of disease. No evidence of inflammatory cell infiltration was observed in rats infected with CRP3 or CRNP5, but an intensive gliosis was present. The brains of CRNP5-infected rats showed severe neuronal degeneration in pyramidal neurons in hippocampus. These results suggest that the cellular immune response to virus infection contributes to BD outcome in CRP3-infected rats but CRNP5-infected rats., P(論文), 特集, application/pdf, FEATURE ARTICLES}, pages = {218--221}, title = {ウイルス性神経障害における発症関連因子の研究}, volume = {13/14}, year = {2007}, yomi = {ニシノ, ヨシイ and マダラマ, ヒロオ and フナバ, マサユキ} }