Elongated versions of Vlp surface lipoproteins protect Mycoplasma hyorhinis escape variants from growth-inhibiting host antibodies
Elongated versions of Vlp surface lipoproteins protect Mycoplasma hyorhinis escape variants from growth-inhibiting host antibodies
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DOI：
10.1128/iai.65.5.1773-1785.1997
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发表时间：
1997-05-01
影响因子：
3.1
通讯作者：
Wise, KS
中科院分区：
文献类型：
--
作者：
Citti, C;Kim, MF;Wise, KS
猪鼻支原体（Mycoplasma hyorhinis）Vlp表面蛋白的变异在决定生物体对宿主抗体（Abs）生长抑制的敏感性方面的作用进行了评估。在这些谱系中，三个基因vlpA、vlpB和vlpC的产物在体外经历相位和大小变化，其通过独立地控制每个vlp基因的表达（启动子突变）或rip基因产物的大小（通过含有串联重复序列的3'区域的基因内扩增或收缩）的不同的增变因子元件发生。通过实验性感染了致关节炎SK76菌株Inflamid、表达较长形式的VlpA、VlpB或VlpC的变体的猪的血清Ab，评估表达不同Vip产物谱的猪鼻病毒SK76对补体非依赖性生长抑制的敏感性（各自单独表达）对宿主免疫血清Ab完全抗性，而表达各Vlp的较短等位基因形式的变体是易感的，生长抑制性Ab的靶标不是Vip产物，因为去除抗Vlp Ab对宿主免疫血清对易感变体的抑制活性没有影响。通过在免疫（相对于对照）宿主血清中繁殖易感变体而衍生的逃逸变体群体显示出对长Vlp表型的强选择，而不管表达的Vlp的身份如何。获得保护性表型的明显突变途径包括表达转录沉默的长rip基因的突变开关或延长表达的vlp基因的开关。这些结果表明，Vip系统的主要功能是保护无壁支原体表面免受能够结合该生物体的重要（和尚未鉴定的）表面抗原的宿主Ab的影响。
Variation in Vlp surface proteins of Mycoplasma hyorhinis was evaluated in terms of its role in determining susceptibility of organisms to growth inhibition by host antibodies (Abs), High-frequency switching of Vip surface lipoproteins has been studied in isogenic lineages of M. hyorhinis SK76, In these lineages, the products of three genes, vlpA, vlpB, and vlpC, are subject to phase and size variation in vitro, which occur through distinct mutator elements that independently govern the expression of each vlp gene (promoter mutations) or the size of the rip gene product (by intragenic expansion or contraction of a 3' region containing tandem repeats), Isogenic clonal variants of M. hyorhinis SK76 expressing distinct profiles of Vip products were assessed for their susceptibility to complement-independent growth inhibition by serum Abs of swine experimentally infected with the arthritigenic SK76 strain, Invariably, variants expressing longer versions of VlpA, VlpB, or VlpC (each expressed individually) were completely resistant to host immune serum Abs, whereas variants expressing shorter allelic versions of each Vlp were susceptible, The target of growth-inhibiting Abs was not the Vip products, since removal of anti-Vlp Abs had no effect on the inhibitory activity of the host immune serum on susceptible variants, Escape variant populations derived by propagating susceptible variants in an immune (versus control) host serum revealed a strong selection for the long-Vlp phenotype, irrespective of the identity of the Vlp expressed. Apparent mutational pathways of acquiring the protective phenotype included mutational switches to express long rip genes that had been transcriptionally silent or switches to elongate expressed vlp genes, These results suggest that a major function of the Vip system is to shield the wall-less mycoplasma surface from host Abs capable of binding vital (and as-yet-unidentified) surface antigens of this organism.