Pal Utpal, Dai Jianfeng, Li Xin, Neelakanta Girish, Luo Phoebe, Kumar Manish, Wang Penghua, Yang Xiuli, Anderson John F, Fikrig Erol
Department of Veterinary Medicine, University of Maryland, College Park, MD 20742, USA.
J Infect Dis. 2008 Jan 1;197(1):148-55. doi: 10.1086/523764.
Borrelia burgdorferi, the etiologic agent of Lyme disease, persists in both an arthropod vector and vertebrate hosts, usually wild rodents. Analysis of the B. burgdorferi transcriptome in vivo indicates that the bb0365 gene is markedly induced as spirochetes enter the feeding ticks from infected mice. To understand the importance of the bb0365 gene product in the spirochete life cycle, we inactivated this gene in an infectious isolate of B. burgdorferi B31. BB0365-deficient spirochetes were fully pathogenic in mice and survived in diverse murine tissues. When naive ticks engorged on spirochete-infected mice, the B. burgdorferi bb0365 mutant entered ticks but had a markedly decreased survival rate compared with wild type B. burgdorferi. BB0365 therefore is not necessary for B. burgdorferi persistence in the vertebrate host but is required for survival of the Lyme disease agent within the feeding arthropod vector, and strategies for interfering with this gene may potentially interrupt the B. burgdorferi life cycle.
莱姆病的病原体伯氏疏螺旋体在节肢动物媒介和脊椎动物宿主（通常是野生啮齿动物）中均能存活。对伯氏疏螺旋体体内转录组的分析表明，当螺旋体从受感染小鼠进入正在吸血的蜱虫时，bb0365基因会被显著诱导。为了解bb0365基因产物在螺旋体生命周期中的重要性，我们在伯氏疏螺旋体B31的一个感染性分离株中使该基因失活。缺乏BB0365的螺旋体在小鼠中具有完全致病性，并能在多种小鼠组织中存活。当未感染的蜱虫吸食感染螺旋体的小鼠血液时，伯氏疏螺旋体bb0365突变体能够进入蜱虫体内，但与野生型伯氏疏螺旋体相比，其存活率显著降低。因此，BB0365对于伯氏疏螺旋体在脊椎动物宿主中的存活并非必需，但对于莱姆病病原体在吸血节肢动物媒介中的存活却是必需的，干扰该基因的策略可能会潜在地中断伯氏疏螺旋体的生命周期。
