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目的:用全基因组重测序方法研究药物干预后耐异烟肼结核杆菌基因突变情况,探讨肺痨康抗耐异烟肼结核杆菌的分子机制与单核苷酸多态性位点(SNPs)的关系。方法:利用全基因组重测序技术对治疗后模型小鼠肺组织中结核杆菌基因组DNA进行重测序,初步筛选变化的SNPs并进行对比分析。结果:肺痨康干预后的PE_PGRS10、PE_PGRS28、frr、PPE54等基因的单核苷酸多态性位点(SNPs)与其他组存在差异。结论:肺痨康抗耐异烟肼肺结核的分子机制可能与其通过干预PE和PPE家族成员,诱导机体产生不同类型和不同程度的免疫反应有关,基因突变所引起的具体生物学变化需要进一步深入探讨。
OBJECTIVE: To study the gene mutation of Mycobacterium tuberculosis isolates of Isoniazid by whole genome resequencing method and to explore the molecular mechanism of resistance to isoniazid-resistant Mycobacterium tuberculosis and single nucleotide polymorphisms (SNPs) . Methods: Genomic DNA of Mycobacterium tuberculosis in the lungs of mice was re-sequenced by whole genome resequencing technique. The SNPs were screened and compared. Results: The single nucleotide polymorphisms (SNPs) of PE_PGRS10, PE_PGRS28, frr, PPE54 and other genes were different from those of other groups after the intervention of Feihe Kang. CONCLUSION: The molecular mechanism of KMT on isoniazid-resistant pulmonary tuberculosis may be related to its mechanism of inducing different types and degrees of immune response through intervention of PE and PPE family members. The specific biological changes caused by gene mutation need to be further explored.