Rosa P A, Schwan T, Hogan D
Laboratory of Microbial Structure and Function, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana 59840.
Mol Microbiol. 1992 Oct;6(20):3031-40. doi: 10.1111/j.1365-2958.1992.tb01761.x.
Borrelia burgdorferi causes Lyme disease, a multisystem illness that can persist in humans for many years. We describe recombination between homologous genes encoding the major outer surface proteins (Osps) A and B of B. burgdorferi which both deletes osp gene sequences and creates chimaeric gene fusions. Recombinant osp genes occur in multiple strains and encode unique proteins that lack some characteristic Osp epitopes. Antigenic variation in Osp through recombination may be relevant to the persistence of B. burgdorferi in an infected host, and has important implications for the utility of OspA and OspB as diagnostic or vaccine candidates for Lyme disease. We also describe Osp variation arising from nonsense mutations and sequence divergence, which may also represent significant sources of Osp polymorphism.
伯氏疏螺旋体可引发莱姆病,这是一种多系统疾病,能在人体内持续多年。我们描述了伯氏疏螺旋体编码主要外表面蛋白(Osps)A和B的同源基因之间的重组,这种重组既能删除osp基因序列,又能产生嵌合基因融合体。重组的osp基因存在于多个菌株中,编码的独特蛋白质缺乏一些特征性的Osp表位。通过重组导致的Osp抗原变异可能与伯氏疏螺旋体在受感染宿主中的持续存在有关,并且对OspA和OspB作为莱姆病诊断或疫苗候选物的效用具有重要意义。我们还描述了由无义突变和序列分歧引起的Osp变异,这也可能是Osp多态性的重要来源。