| ［1］Nair N, Cooreman E. Working towards TB elimination the WHO Regional strategic Plan(2006—2015). J Commum Dis, 2006, 38（3）:185-190. ［2］Rustad TR, Sherrid AM, Minch KJ, et al. Hypoxia: a window into Mycobacterium tuberculosis latency. Cell Microbiol, 2009, 11（8）:1151-1159. ［3］Mccune RM Jr, Mcdermott W, Tompsett R.The fate of Mycobacterium tuberculosis in mouse tissues as determined by the microbial enumeration technique. II. The conversion of tuberculous infection to the latent state by the administration of pyrazinamide and a companion drug. J Exp Med, 1956, 104(5):763-802. ［4］Wayne LG. Dormancy of Mycobacterium tuberculosis and latency of disease. Eur J Clin Microbiol Infect Dis, 1994, 13 (11): 908-914. ［5］郭利民，张廷芬，师长宏,等.结核分枝杆菌潜伏性感染的诊断.医学杂志研究, 2009, 38 (4): 7-9.［6］Vergne I, Chua J, Deretic V. Tuberculosis toxin blocking phagosome maturation inhibits a novel Ca2+/calmodulin-PI3K hVPS34 cascade. J Exp Med, 2003, 198 (4): 653-659. ［7］Park HD,Guinn KM,Harrell MI,et a1. Rv3133c／dosR is a transcription factor that mediates the hypoxic response of Myeobacterium tuberculosis. Mol Microbiol,2003, 48(3)：833-843. ［8］李青，姜雯雯，雒彧，等.结核分枝杆菌抗原Ag85B-Mpt64 190-198-HspX融合蛋白免疫原性的初步观察.中华微生物学和免疫学杂志, 2009, 29(2): 103-107.［9］苏华，付玲，朱红艳,等. 肾小球疾病间质泡沫细胞的分布及其临床病理意义. 临床与实验病理学杂志，2009, 25(6): 606-609. ［10］Peyron P, Vaubourgeix J, Poquet Y,et al. Foamy Macrophages from Tuberculous Patients’ Granulomas Constitute a Nutrient-Rich Reservoir for M.tuberculosis Persistence. PLoS Pathog, 2008, 4 (11): e1000204.［11］Fu X, Jiao W, Chang Z. Phylogenetic and biochemical studies reveal a potential evolutionary origin of small heat shock proteins of animals from bacterial class A. J Mol Evol, 2006, 62(3): 257-266. ［12］Chen X,Fu X,Ma Y,et al. Chaperone-like activity of Mycobacterium tuberculosis Hsp16.3 does not require its intact (native) structures. Biochemistry (Mosc),2005,70(8):913-919. ［13］Fu X, Chang Z. Identification of a highly conserved pro-gly doublet in non-animal small heat shock proteins and characterization of its structural and functional roles in Mycobacterium tuberculosis Hsp 16.3. Biochemistry, 2006, 71(1): 68-73. ［14］刘忠华,丁元生, 毕爱笑，等.结核分枝杆菌38kD-16kD融合蛋白克隆表达及血清学诊断价值. 中国防痨杂志, 2009, 31(10): 565-568.［15］Geluk A, Lin MY, van Meijgaarden KE, et al. T-cell recongnition of the HspX protein of Mycobacterial tuberculosis correlates with latent M.tuberculosis infection but not with M.bovis BCG vaccination. Infect Immun, 2007, 75(6): 2914-2921. ［16］Cunningham AF, Spreadbury CL. Mycobacterial tionary phasee induced by low oxygen tension：cell wall thickening and localization of the 16-kilodalton alpha-crystallin homlog.J Bacteriol, 1998, 180(4): 801-808. ［17］Wang Z,Cao AN,Lai LH. High activity of Mj HSP 16.5 under acidic condition. Sci China Ser B, 2009, 52(3): 325-331.［18］Sirkar M, Majumdar S. Lipoarabinomannaninduced cell signaling involves ceramide and mitogen-activated protein kinase. Clin Diagn Lab Immunol, 2002, 9(6): 1175-1182. ［19］Song CH, Lee JS, Lee SH, et al. Role of mitogen-activated protein kinase pathways in the production of tumor necrosis factor-alpha,interleukin-10,and monocyte chemotactic protein1 by Mycobacterium tuberculosis H37Rv-infected human monocytes.J Clin Immunol, 2003, 23(3): 194-201. ［20］孙逊, 蒋超英. 结核蛋白芯片对肺结核球及肺门淋巴结结核与其他肺部占位病变的诊断价值. 中国防痨杂志, 2010, 32(7): 405-407.［21］Chan J, Fan XD, Hunter SW,et al. Lipoarabinomannan,a possible virulence factor involved in persistence of Mycobacterium tuberculosis within macrophages.Infect Immun, 1991, 59(5): 1755-1761. ［22］Roach TI, Barton CH, Chatterjee D,et al.Macrophage activation:lipoarabinomannan from avirulent and virulent strains of Mycobacterium tuberculosis differentially induces the early genes cfos,KC,JE,and tumor necrosis factoralpha. J Immunol, 1993, 150(5): 1886-1896. ［23］Li JM，Li N，Zhu DY, et al. Isocitrate lyase from Mycobacteria tuberculosis promotes survival of Mycobacterium smegmatis within macrophage by suppressing cell apoptosis. Chin Med J(Engl), 2008, 121(12): 1114-1119. ［24］Graham JE，Clark-Curtiss JE. Identification of Mycobacterium tuberculosis RNAs synthesized in response to phagocytosis by human macrophages by selective capture of transcribed sequences (SCOTS). Proc Natl Acad Sci U S A, 1999，96(20):11554-11559.［25］Shiloh MU, DiGiuseppe Champion PA. To catch a killer. What can mycobacterial models teach us about Mycobacterium tuberculosis pathogenesis? Curr Opin Microbio,2010,13 (1): 86-92. ［26］罗开军, 石君, 王晓红,等. 结核分枝杆菌休眠期和活跃期差异表达基因分析. 中国病原生物学杂志, 2010,(12):889-895.［27］刘一典,肖和平,沙巍,等. 新发和复发肺结核维生素D受体基因多态性分布. 中国感染与化疗杂志, 2008,(04):289-292.［28］DeMaio J, Zhang Y, Ko C，et al.A stationary-phase stress-response sigma factor from Mycobacterium tuberculosis. Proc Natl Acad Sci U S A,1996,93(7):2790-2794. ［29］袁群英. 抗结核病药物治疗的研究进展. 临床肺科杂志, 2010,(05):701-703.［30］Murphy DJ, Brown JR. Identification of gene targets against dormant phase Mycobacterium tuberculosis infection. BMC Infect Dis, 2007, 7: 84. ［31］Mukamolova GV, Turapov OA, Kazarian K, et a1.The rpf gene of Micrococcus luteus encodes an essential secreted growth factor.Mol Microbiol, 2002, 46(3): 611-621. ［32］Biketov S, Potapov V, Ganina E, et al. The role of resuscitation promoting factors in pathogenesis and reactivation of Mycobacterium tuberculosis during intra-peritoneal infection in mice. BMC Infect Dis, 2007, 7:146. ［33］Kana BD, Gordhan BG, Downing KJ, et al. The resuscitation-promoting factors of Mycobacterium tuberculosis are required for virulence and resuscitation from dormancy but are collectively dispensable for growth in vitro. Mol Microbiol， 2008, 67（3）: 672-684. ［34］Hett EC, Chao MC, Steyn AJ,et al. A partner for the resuscitation-promoting factors of Mycobacterium tuberculosis. Mol Microbiol, 2007, 66（3）:658-668. |
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