Abstract:Objective:To investigate the association between katG, inhA and AhpC gene mutations and isoniazid (INH) resistance of Mycobacterium tuberculosis (MTB) in this region.Methods:The results of pre-anti-tuberculosis Mycobacterium tuberculosis (MTB) culture and drug resistance gene detection in hospitalized tuberculosis patients from January 2019 to December 2021 in the Department of Tuberculosis of our hospital were retrospectively analyzed.Results:MTB culture in sputum or lavage fluid and strain identification were performed in 1712 cases of Mycobacterium humantype, 1308 cases were sensitive to INH phenotype and 404 cases were drug-resistant. At the same time, 663 samples were also tested for INH resistance gene (molecular drug sensitivity), 99 cases were not detected, 564 cases were positive for molecular drug sensitivity, among which 390 cases were sensitive and 174 cases were mutated, and the mutation sites were katG315, inhA promoter and AhpC promoter. With phenotypic drug sensitivity as the gold standard, molecular drug sensitivity detected INH drug resistance sensitivity of 92.4% (95%CI: 88.5%-96.4%) specificity of 96.2% (95%CI: 94.3%-98.1%), positive predictive value of 91.4% (95%CI: 87.2%-95.5%) negative predictive value was 96.7% (95%CI: 94.9%-98.4%), the index was 88.6%, and the accuracy was 95%. Among 172 phenotypic drug-resistant patients, 159 cases of drug-resistant gene mutations were detected, including 126 katG315 mutations, 25 inhA promoter mutations and 15 AhpC promoter mutations, respectively. The incidence of katG315 mutations was significantly higher than that of inhA and ahpC promoters (X2= 123.9 and 151.8, P < 0.001). Forty-one katG315 mutations, eight inhA promoter mutations and five ahpC promoter mutations were detected in 52 patients with high phenotype resistance (MIC≥10μg /ml). The katG315 mutation rate was significantly higher than that of inhA and ahpC promoter (X2 = 28.0 p < 0.001). The high drug resistance rate of katG315 combined with inhA or ahpC promoter mutation was significantly higher than katG315 alone mutation (X2 = 4.951, P=0.045). The mutation rate of katG315 in MDR and quasi-extensively resistant groups was significantly higher than that in isoniazid-resistant groups (X2= 5.522, p=0.018; X2=8.422, P=0.007). The mutation rate of katG315 combined with inhA/ahpC promoter was significantly increased in the quasi-extensively resistant group (X2=8.916, P=0.006). Conclusions:katG315 is the main mutation site of isoniazid resistance in this region, which is closely related to isoniazid resistance and the degree of resistance.