POINT MUTATION IN MENINGOCOCCAL POR-A GENE ASSOCIATED WITH INCREASED ENDEMIC DISEASE
POINT MUTATION IN MENINGOCOCCAL POR-A GENE ASSOCIATED WITH INCREASED ENDEMIC DISEASE
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DOI：
10.1016/0140-6736(91)91297-8
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发表时间：
1991-03-02
期刊：
影响因子：
168.9
通讯作者：
HECKELS, JE
中科院分区：
文献类型：
--
作者：
MCGUINNESS, BT;CLARKE, IN;HECKELS, JE
por A 基因编码脑膜炎球菌 1 类外膜蛋白的表达，负责抗原亚型特异性，已在格洛斯特地区一名脑膜炎球菌性脑膜炎患者的脑膜炎奈瑟菌 (B:15:P1.7,16) 分离株中进行克隆和测序。 该序列与 P1.7,16 参考菌株的等效基因的序列比较揭示了点突变，该突变在负责 P1.16 特异性的表位中产生单个氨基酸变化。 具有 P1.16 特异性的单克隆抗体不会与与改变的表位相对应的合成肽发生反应，并且不会促进补体介导的分离株杀菌作用。对其他菌株的分析表明，在英格兰和威尔士，由于 B:15:P1.7,16 脑膜炎球菌（具有改变的表位 (P1.16b)）引起的感染广泛分布。
The por A gene, which encodes expression of meningococcal class 1 outer membrane protein, responsible for antigenic subtype specificity, has been cloned and sequenced in an isolate of Neisseria meningitidis (B:15:P1.7,16) from a patient in the Gloucester area with meningococcal meningitis. Comparison of the sequence with that of the equivalent gene from the P1.7,16 reference strain reveals a point mutation which generates a single amino acid change in the epitope responsible for P1.16 specificity. Monoclonal antibodies with P1.16 specificity do not react with synthetic peptides that correspond to the altered epitope, and do not promote complement-mediated bactericidal killing of the isolate. Analysis of other strains shows widespread distribution of infections due to B:15:P1.7,16 meningococci with the altered epitope (P1.16b) in England and Wales.