脑膜炎球菌porA基因的点突变与局域性疾病增加有关
B T McGuinness1, I N Clarke, P R Lambden
1Department of Microbiology, University of Southampton Medical School, UK.
Lancet (London, England)
|March 2, 1991
概括
尼塞利亚脑膜炎 porA 基因的突变改变了 P1.16 表位,影响了抗体识别和补充介导杀死. 这种改变的菌株 (P1.16b) 在英格兰和威尔士普遍存在.
科学领域:
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
- 遗传学 是一个遗传学.
背景情况:
- 细菌性脑膜炎是由Neisseria meningitidis引起的.
- porA基因编码了1类外膜蛋白,对抗原特异性至关重要.
- 脑膜炎球菌血清组B,亚型P1.7,16,是感染的重要原因.
研究的目的:
- 从Neisseria meningitidis (B:15:P1.7,16) 的临床分离物中克隆和测序 porA 基因.
- 调查脑膜炎球菌菌株抗原特异性变化的遗传基础.
- 为了确定脑膜炎球菌菌株的流行率,具有特定的表皮图变化.
主要方法:
- 基因克隆和 porA 基因的 DNA 测序.
- 测序基因与参考菌株的比较.
- 使用单克隆抗体和合成类的皮质分析.
- 评估补充介导的杀菌活性.
主要成果:
- 鉴定出porA基因的一个点突变,导致P1.16表位组中的单个氨基酸变化.
- 对P1.16特异的单克隆抗体没有与改变表位的反应.
- 改变的表位 (P1.16b) 使该分离物耐受于补充介导的杀菌.
- 在英格兰和威尔士,由P1.16b表观素引起的Neisseria meningitidis感染很普遍.
结论:
- 发现的porA基因突变是导致Neisseria meningitidis中P1.16表位变化的原因.
- 这种表位变化会影响免疫识别和宿主防御机制.
- 带有P1.16b表位的菌株的广泛分布突显了其流行病学意义.
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