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Genetic stability of Borrelia burgdorferi recovered from chronically infected immunocompetent mice.

机译:从慢性感染的有免疫能力的小鼠中回收伯氏疏螺旋体的遗传稳定性。

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Persistent infection with Borrelia burgdorferi in the presence of a vigorous host immune response has been demonstrated in humans and in animal models of Lyme disease. Long-term persistence of B. burgdorferi was documented recently in our studies of BALB/c and C3H mice infected with cloned and uncloned strains of B. burgdorferi. From mice inoculated with the cloned strain, 11 isolates were recovered from the skin, bladder, and blood after 1 year of infection. Analysis of the genes encoding the major outer surface proteins (OspA and OspB) by restriction digestion and DNA sequencing showed no evidence of point mutations or other small genetic alterations after 1 year. Genomic macrorestriction analysis of whole B. burgdorferi showed no loss or gross alterations of the plasmids encoding OspA, OspB, or OspC. However, in two isolates, loss of a 38-kb plasmid encoding outer surface protein D was noted. Our studies suggest that loss or alteration of the genes encoding OspA and OspB is not a common occurrence during persistent spirochetal infection and that other possible mechanisms, including invasion of immunologically privileged sites, should be actively explored.
机译:在人类和莱姆病的动物模型中,已证明在强烈的宿主免疫反应下持久存在伯氏疏螺旋体感染。最近,在我们对克隆和未克隆的伯氏疏螺旋体菌株感染的BALB / c和C3H小鼠的研究中,伯氏疏螺旋体长期持续存在。从感染了该克隆菌株的小鼠中,感染1年后,从皮肤,膀胱和血液中回收了11种分离株。通过限制性酶切和DNA测序对编码主要外表面蛋白(OspA和OspB)的基因进行分析,发现没有证据表明在1年后出现点突变或其他小的遗传改变。整个伯氏疏螺旋体的基因组宏观限制性分析表明,编码OspA,OspB或OspC的质粒没有丢失或发生总体改变。然而,在两个分离物中,注意到编码外表面蛋白D的38kb质粒的丢失。我们的研究表明,在持续性螺旋体感染期间,编码OspA和OspB的基因的丢失或改变并不常见,因此应积极探索其他可能的机制,包括入侵具有免疫功能的位点。

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