结核分枝杆菌Rv2660c蛋白结构分析及抗原表位预测

目的 分析结核分枝杆菌Rv2660c蛋白的结构并预测其抗原表位,为研发针对结核潜伏性感染的治疗性疫苗和药物提供新的靶点。方法 用BLAST软件分析Rv2660c蛋白与人类蛋白的同源性,然后运用生物信息学方法预测其二级结构、跨膜结构、信号肽序列及T细胞和B细胞抗原表位。结果 BLAST结果显示,Rv2660c蛋白与人类蛋白同源性不高,同源性最高的人类蛋白是MAD 6蛋白,同源性仅为16%。Rv2660c蛋白无跨膜区,为胞外蛋白,不含信号肽序列;该蛋白含丰富的B细胞和T细胞抗原表位,19-35、48-54、28-44和58-73位氨基酸残基可能存在优势线性B细胞表位;56-64位和65-74位氨基酸可能存在优势辅助性T细胞表位,66-74、41-49、63-71位氨基酸可能存在优势细胞毒性T细胞表位。结论 Rv2660c蛋白含丰富抗原表位,具有较强的体液免疫和细胞免疫原性,可望作为潜伏性感染结核的治疗性疫苗和药物的作用靶点。

Structure analysis and epitopes prediction of Mycobacterium tuberculosis Rv2660c protein

Objective To promote a new target of developing therapeutic vaccines and drugs against latent mycobacterium tuberculosis infection by analyzing the structure and predicting the epitopes of Mycobacterium tuberculosis Rv2660c protein.Methods Blast software analysis was used to assess the homology between Rv2660c protein and human protein,and bioinformatics methods were used to predict the secondary structures,transmembrane structures,signal peptide sequences,epitopes of T cell and B cell.Results Blast result showed that Rv2660c protein had low homology with human protein.Human MAD 6 protein has the highest homology with Rv2660c protein,but the homology was only 16%.Rv2660c protein has no transmembrane regions nor signal peptide sequences and had rich B cell and T cell epitopes.Epitopes prediction showed that 19-3548-5428-44 and 58-73 amino acid residues might be potential B cell epitopes.This nucleic region is mostly composed with beta angle and irregular coil structure,showing higher hydrophilicity,surface probability,and flexibility.Besides,56-64 and 65-74 amino acid residues might be potential supporting T cell epitopes and 66-7441-4963-71 amino acid residues might be potential cytotoxic T lymphocyte epitopes.Conclusion Rv2660c protein contains abundant epitopes and was potential to elicit prominent cellular immune responses and strong humoral immunity,suggesting that Rv2660c protein was a potential target to develop new vaccines and drugs to control latent mycobacterium tuberculosis infection.