Dyet Kristin H, Martin Diana R
Communicable Disease Group, Institute of Environmental Science and Research, Porirua, New Zealand.
J Clin Microbiol. 2005 Feb;43(2):838-42. doi: 10.1128/JCM.43.2.838-842.2005.
Since mid-1991, New Zealand has experienced an epidemic of meningococcal disease. The epidemic has been caused by serogroup B meningococci expressing PorA type P1.7-2,4, belonging to the ST-41/ST-44 complex, lineage III. Most B:P1.7-2,4 meningococci express type 4 PorB (87.0%), although case isolates with porB other than type 4 have been identified throughout the duration of the epidemic. To assess the genetic relatedness of case isolates with an alternative porB gene, multilocus restriction typing validated against multilocus sequence typing was used. This determined that B:P1.7-2,4 meningococci with a porB gene that was other than type 4 had the same clonal origin. It was concluded that strains with alternative porB genes had diverged from the original type 4 porB. Variation in porB was also shown to be associated with the uptake of DNA encoding one or two of the PorB variable regions leading to mosaic porB. Point mutation rather than horizontal transfer and recombination was implicated as the mechanism of sequence variation in some strains. This work will serve as a reference point to determine if the administration of a strain-specific vaccine increases the level of porB divergence and variation already observed in New Zealand case isolates. It also complements the study undertaken of PorA stability which showed that variation in P1.7-2,4 PorA was almost exclusively due to deletions in the P1.4 epitope of the epidemic strain.
自1991年年中以来,新西兰经历了一场脑膜炎球菌病疫情。该疫情由表达PorA型P1.7-2,4的B群脑膜炎球菌引起,属于ST-41/ST-44复合体,III型谱系。大多数B:P1.7-2,4脑膜炎球菌表达4型PorB(87.0%),尽管在疫情期间已鉴定出携带非4型porB的病例分离株。为了评估携带替代porB基因的病例分离株的遗传相关性,使用了针对多位点序列分型验证的多位点限制性分型。这确定了携带非4型porB基因的B:P1.7-2,4脑膜炎球菌具有相同的克隆起源。得出的结论是,携带替代porB基因的菌株已从原始的4型porB分化而来。还表明porB的变异与编码一个或两个PorB可变区的DNA摄取有关,导致镶嵌型porB。一些菌株的序列变异机制被认为是点突变而非水平转移和重组。这项工作将作为一个参考点,以确定使用菌株特异性疫苗是否会增加在新西兰病例分离株中已经观察到的porB分化和变异水平。它还补充了对PorA稳定性的研究,该研究表明P1.7-2,4 PorA的变异几乎完全是由于流行菌株P1.4表位的缺失。