Achtman M, Kusecek B, Morelli G, Eickmann K, Wang J F, Crowe B, Wall R A, Hassan-King M, Moore P S, Zollinger W
Max-Planck Institut für molekulare Genetik, Berlin, Germany.
J Infect Dis. 1992 Jan;165(1):53-68. doi: 10.1093/infdis/165.1.53.
Serogroup A Neisseria meningitidis of subgroup III has caused two pandemics of meningococcal meningitis since 1966 and recently spread to East Africa. The last epidemics in West Africa in the early 1980s were caused by clone IV-1. Surface antigens of clone IV-1 strains from West Africa and subgroup III strains from both pandemic waves were analyzed. Lipopolysaccharide was stable within clone IV-1 but variable in subgroup III. Pili from clone IV-1 possessed class I epitopes, while those from subgroup III also possessed class IIa epitopes. Certain class 5 protein variants were expressed by both bacterial clones, possibly reflecting either inheritance of primeval genes or horizontal transmission. Exposure of Gambians to clone IV-1 bacteria stimulated production of bactericidal antibodies cross-reactive with subgroup III bacteria in some individuals but of type-specific antibodies in others. Gambians without bactericidal antibodies usually became healthy carriers rather than developing meningococcal disease on exposure to virulent meningococci.
自1966年以来,III亚群的A群脑膜炎奈瑟菌已引发了两次脑膜炎球菌性脑膜炎大流行,最近传播到了东非。20世纪80年代初在西非的最后几次流行是由IV-1克隆株引起的。对来自西非的IV-1克隆株和两次大流行浪潮中的III亚群菌株的表面抗原进行了分析。脂多糖在IV-1克隆株内稳定,但在III亚群中可变。IV-1克隆株的菌毛具有I类表位,而III亚群的菌毛也具有IIa类表位。两个细菌克隆株都表达了某些5类蛋白变体,这可能反映了原始基因的遗传或水平传播。冈比亚人接触IV-1克隆株细菌后,在一些个体中刺激产生了与III亚群细菌交叉反应的杀菌抗体,而在另一些个体中则产生了型特异性抗体。没有杀菌抗体的冈比亚人在接触有毒力的脑膜炎球菌后通常成为健康携带者,而不是患上脑膜炎球菌病。