In vitro Molecular analysis and studying the factors affecting subclinical forms of Mycobacterium

Abstract

Tuberculosis is the historic but infectious disease which can be curable with little effort. It is affecting the world’s population due to the drug resistance that is acquiring by the Mycobacterium tuberculosis. However, with the study of the domains those are involved in the drug resistance one can excel and move towards biopharming and drug formation which will be more efficient. Subclinical form of tuberculosis is majorly found in every individual but due to the presence of different environmental factors this form changes into pathogenic form and starts causing disease. In a nut shell one must say that the major factor triggering the subclinical form to become clinical form is smoking, which accounts for 65%, living conditions accounts for 56% and gender of a person accounts for 62% in changing the subclinical form into active TB disease; some how age also have its impact over progression of disease. In our study blood serum of 400 patients were taken for diagnostic analysis using polymerase chain reaction (PCR). From these samples, 300 patients were found to be positive for TB; and from these positive samples 184 (61.3%) found to be drug resistant. Our data suggest that the Mycobacterium tuberculosis is becoming resistant towards the major drugs that are currently being used as Isoniazid, rifampicin, pyrazinamide, ethambutol and streptomycin due to various factors. To overcome that problem the major genes of Mycobacterium tuberculosis that are targeted sites for drug action were analyzed using different databases. Specific domains were found that intract with drugs and mutations in these sites which leads towards the drug resistant. In this study we also analyzed 11 genes ( KatG,inhA, rpoB, pncA, embB, rrs, gidB, tlyA, gyrA, gyrB, thyA) along with their domains were analyzed. Out of these 12 genes eight genes were found to be the targeted sites for drug binding i.e. gyrA, gyrB, tlyA, gidB, rrs, embB,rpoB, inhA.