ORIGINAL RESEARCH

Isoniazid-resistant Mycobacterium tuberculosis: prevalence, resistance spectrum and genetic determinants of resistance

About authors

Laboratory of Biotechnology, Central Tuberculosis Research Institute, Moscow, Russia

Correspondence should be addressed: Sofia N. Andreevskaya
Yauzskaya alley, 2, Moscow, 107564; ur.liam@aifosdna

About paper

Funding: this study was supported by the Ministry of Science and Higher Education of the Russian Federation and carried out under the Federal Targeted Program for Research and Development in Priority Areas of Development of the Russian Scientific and Technological Complex for 2014-2020, Project № 05.586.21.0065 (Project ID RFMEFI58619X0065).

Author contribution: Ergeshov A, Chernousova LN — study design; Larionova EE, Andrievskaya IYu — data acquisition; Smirnova TG — data analysis; Andreevskaya SN — manuscript preparation, literature analysis. All authors have equally contributed to the discussion of the obtained results.

Received: 2019-12-11 Accepted: 2020-01-07 Published online: 2020-01-12
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Table 1. M. tuberculosis isolates and drug susceptibility tests
Note: 1 — including cases for which no mutations were detected in the genes associated with resistance to isoniazid, rifampicin and fluoroquinolones; 2 — including 38 M. tuberculosis isolates for which no mutations in the rpoB gene (see the article) were detected; 3 — including 29 M. tuberculosis isolates carrying mutant rpoB but having no resistance phenotype; 4 — mono- or polyresistance to antituberculous drugs, excluding isoniazid.
Table 2. The frequency of detection of isoniazid-resistant M. tuberculosis in 2011–2018
Table 3. Resistance spectra of isoniazid-resistant strains of M. tuberculosis
Note: in the lists of resistance spectra, first-line drugs are separated from second- line medications by a space character.
Table 4. Isoniazid-resistant M. tuberculosis isolates with different combinations of mutations in the genes associated with isoniazid resistance
Note: SNPs occurring in only one gene associated with isoniazid resistance are highlighted in gray; other cells show combinations of >1 mutation. * Thr(1) represents the AGC->ACC substitution, Ser->Thr(2) represents the AGC->ACA substitution.