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Summer Research Fellowship Programme of India's Science Academies

Pharmacogenomics in tuberculosis

Richa Prakash

Central University of Punjab, Mansa Road, Bathinda 151001

Dr. Ranjan Nanda

Group Leader, Translational Health Group, International Centre for Genetic Engineering and Biotechnology (ICGEB), Aruna Asaf Ali Marg, New Delhi 110067

Abstract

Tuberculosis is the second major cause of death from infectious disease around the world after AIDS. India is among 15 countries having highest tuberculosis incidence rates. According to 2017 WHO reports, there were 10 millions new cases of tuberculosis and 1.6 million death due to tuberculosis including 0.3 million HIV positive cases. Tuberculosis is caused by an aerobic non-motile bacillus characteristically acid-fast due to high lipid content of their cell wall, Mycobacterium tuberculosis (Mtb). Generally, it affects the Lungs (Pulmonary Tuberculosis) but it can affect any part of the body (Extra-pulmonary Tuberculosis) and it spreads through air by active tuberculosis patients only. Most tuberculosis infections are latent in nature, i.e. they are asymptomatic having 10% chances of their conversion into active tuberculosis. Pharmacogenomics deals with interindividual variability to drug response or in simpler words, it is the study of "Drug-Genome interactions". It aims to optimize effective and safe medication according to the genetic makeup of the individual. From over 50 years, tuberculosis is being treated with combination drug therapy because the causative agent Mtb becomes resistant to single drug therapy. The treatment regimen of tuberculosis generally includes treatment with isoniazid, rifampicin, pyrazinamide and ethambutol for 2 months and then isoniazid and rifampicin for next 4 months. This treatment is effective in >95% in patients having susceptible tuberculosis strains and have a relapse of <5%. So, pharmacogenomics study of drugs involved in the treatment of tuberculosis can help understand the variation in drug response by different individuals by analysing any polymorphism found in their genetic makeup.

Keywords: Mycobacterium tuberculosis, Glutathione-S-transferases, anti-tuberculosis drug-induced hypertoxicity, isoniazid, rifampicin

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