作者: Sue A. Theus , M. Donald Cave , Kathleen D. Eisenach
DOI: 10.1007/978-1-59745-569-5_9
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摘要: Tuberculosis (TB) remains a global public health crisis despite being curable disease (1) . Access to the complete genomic sequence of Mycobacterium tuberculosis (MTB) laboratory strain H37Rv and clinical isolate CDC1551 has facilitated investigations into pathogenicity MTB. However, mycobacterial factors that contribute virulence MTB or modulate interaction this pathogen with human host are only beginning be elucidated. Despite previous studies suggesting an extremely low mutation rate, there compelling reasons suspect strain-specific attributes directly outcome. Our infections in THP-1 cells epidemiologically distinct strains provide strong evidence specific may differentially pathogenic (2 , 3) Clinical associated TB outbreaks grow significantly faster macrophages than do non-outbreak strains. The rapid growth demonstrated by was highly correlated production interleukin (IL)-10 suppression tumor necrosis factor (TNF)-α. These results suggest enhanced capacity rapidly is marker virulence, certain attributed downregulation Th1type immune response. ability combine information pathogenesis employing diverse will enable us continue unravel molecular basis identify influence presentation, outcome (treatment failure, relapse, development drug resistance), transmission infection. Ultimately, having relevant characteristics could potentially impact how we treat control spread elucidate whether protection afforded new candidate vaccine.