Genomic and clinical factors associated with drug-resistant tuberculosis

Background Drug-resistant tuberculosis is a significant global health issue caused by mutations in Mycobacterium tuberculosis , the infectious agent of the disease. WHO’s End TB Strategy mandates drug susceptibility testing for rifampicin in all confirmed tuberculosis cases and fluoroquinolone testing for rifampicin-resistant cases. Objective The review aims to analyse Mycobacterium tuberculosis genome mutations; Clinical factors linked to drug resistance. Major thematic findings: The mutant otsB1 trehalose-6-phosphate phosphatase shows rifampicin resistance in hypoxic conditions. Pyruvate dehydrogenase E2 is vital for RNI resistance, host cell death, and Mycobacterium tuberculosis growth. Individuals with drug-susceptible tuberculosis showed higher plasma levels of inducible nitric oxide synthase. NO and iNOS expression can be influenced by factors other than mycobacterial infection. Activated macrophages convert L-arginine to NO via TNF-α and IFN-γ. Serum L-arginine levels were measured in individuals with pulmonary tuberculosis, their household contacts, and healthy controls. PPE51, PE15, and PE20 improve drug resistance by transporting metal ions and absorbing nutrients. In diagnosis, the CRISPR-guided mutagenic DNA polymerase identifies changes in drug-resistant Mycobacterium tuberculosis . Mycobacterium smegmatis , recognized for its rapid growth, and the slow-growing Mycobacterium tuberculosis were evaluated using CRISPR-guided DNA polymerase. Also, machine learning and whole-genome sequencing predicted isoniazid, Rifampicin, and multidrug-resistant tuberculosis with 90% precision. The BDQ DILI network can offer valuable support on monitor the adverse events of the Anti-tuberculosis therapy. Conclusion Whole genome sequencing, tNGS, and deletion-targeted multiplex PCR effectively detect mutations. Studying PE/PPE genes offers a key chance to drug-resistant tuberculosis research and improve tuberculosis treatment outcomes.