RIF resistance due to mutations in the rpoB gene, the gene that produces RNA polymerase β-subunit and INH resistance is largely due to mutations in the gene katG. With the increasing number of people with HIV/AIDS cause TB disease, WHO categorizes as a re-emerging disease. Objective of this study was to obtain information MDR-TB relations with the relevant genes, as well as information combined genotype of M. tuberculosis. Here, we reported that their C1363A nucleotide changes (Pro535His) in M. tuberculosis sensitive six antituberculosis drugs showed entire rpoB mutations causing resistance properties. On the basis of this phenomenon, it can be suggested that the formation mechanism of MDR-TB strains begins with rpoB mutations followed by mutation katG. This study shows that the mechanism of resistance to an anti-tuberculosis drug that only affects a single gene, such as rifampin affecting rpoB, will be more easily controlled than anti-tuberculosis drugs that affect multiple genes, for example isoniazid affecting other genes other than katG. The analysis showed a residue that forms a bond with a hydroxyl group of RIF will provide the most impact when there is a change of amino acid residues. Ser411 residue (531 homolog in M. tuberculosis), has the shortest distance to the RIF and form bonds. Changes in the amino acid residues have caused the greatest effect on the phenotype of M. tuberculosis. The change of leucine amino acid serine be causing changes in the bond and also the distance between the amino acid residues with the RIF. It is visible at the level of resistant isolates have mutations rpoB531 relatively higher compared to other mutations in codon rpoB.
