抗酸菌の休眠現象や薬剤抵抗性に関わる分子メカニズム

Abstract

Instead of rapid multiplication, pathogenic mycobacteria, such as Mycobacterium tuberculosis are likely to have acquired slow but long life. Host immunity affords desirable non-competitive environment for M tuberculosis in human lungs, where this pathogen slowly grows or arrests growing, which avoids rapid loss of living places. Mycobacterial DNA-binding protein 1 (MDP1), a unique histone-like protein associating mycobacterial GC-rich DNA, has pivotal role in realizing such slow life and pathogenesis including drug tolerance to isoniazid.