Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, Division of Intramural Research, National Institute of Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA.
Infect Immun. 2011 Sep;79(9):3510-7. doi: 10.1128/IAI.05014-11. Epub 2011 Jun 27.
Borrelia burgdorferi, the causative agent of Lyme disease, exists in a complex enzootic cycle, transiting between its vector, Ixodes ticks, and a diverse range of vertebrate hosts. B. burgdorferi linear plasmid 38 (lp38) contains several genes that are differentially regulated in response to conditions mimicking the tick or mouse environments, suggesting that these plasmid-borne genes may encode proteins important for the B. burgdorferi infectious cycle. Some of these genes encode potential virulence factors, including hypothetical lipoproteins as well as a putative membrane transport system. To characterize the role of lp38 in the B. burgdorferi infectious cycle, we constructed a shuttle vector to selectively displace lp38 from the B. burgdorferi genome and analyzed the resulting clones to confirm the loss of lp38. We found that, in vitro, clones lacking lp38 were similar to isogenic wild-type bacteria, both in growth rate and in antigenic protein production. We analyzed these strains in an experimental mouse-tick infectious cycle, and our results demonstrate that clones lacking lp38 are fully infectious in a mouse, can efficiently colonize the tick vector, and are readily transmitted to a naive host.
伯氏疏螺旋体，莱姆病的病原体，存在于一个复杂的动物媒介传染病循环中，在其媒介，硬蜱和多种脊椎动物宿主之间转移。伯氏疏螺旋体线性质粒 38（lp38）包含几个基因，这些基因在模拟蜱或鼠环境的条件下差异调控，表明这些质粒携带的基因可能编码对伯氏疏螺旋体感染循环至关重要的蛋白质。其中一些基因编码潜在的毒力因子，包括假设的脂蛋白和一个假定的膜转运系统。为了表征 lp38 在伯氏疏螺旋体感染循环中的作用，我们构建了一个穿梭载体，选择性地从伯氏疏螺旋体基因组中置换 lp38，并分析产生的克隆以确认 lp38 的缺失。我们发现，在体外，缺失 lp38 的克隆与同源野生型细菌相似，在生长速度和抗原蛋白产生方面都相似。我们在实验性的鼠-蜱感染循环中分析了这些菌株，结果表明，缺失 lp38 的克隆在小鼠中具有完全的感染力，能够有效地定殖蜱媒介，并容易传播给未感染的宿主。
