Antimicrobial-resistant infections have become an alarming threat to public health. Drug-resistant tuberculosis (TB) is a particularly widespread issue that can be especially damaging or fatal. A recently-published study identified a “survival gene” that prevents TB strains from becoming multiresistant.
One third of the world’s population has TB, according to the CDC, and 1.8 million TB-related deaths worldwide were recorded in 2015. Mismanagement of antibiotic treatment and person-to-person transmission have contributed to the emergence of TB superbugs, and in some countries, it has become increasingly difficult to treat.
The study, published in Nature Communications, presents findings that may contribute to better understanding the mechanisms of drug-resistant TB. The survival gene identified by researchers, called NucS, can significantly decrease mutation rates in infectious, TB-causing mycobacteria. The researchers screened the growth of mutant strains on rifampicin, and discovered a DNA repair enzyme produced by the gene that halts mutation activity.
Genetic variations found in NucS are also able to influence mutation rates in clinically isolated strains of mycobacteria, leading researchers to note that these results may bring scientists closer to improving treatment options.  
“Not only does this study identify that mutations can be reversed in mycobacteria,” Professor Jesus Blazquez, from the Centro Nacional de Biotecnologia, said in a press release, “it reveals that the loss of this DNA repair process can cause a huge increase in the mutation rates, significantly increasing the likelihood of these pathogens acquiring mutations – which can cause antibiotic resistance.”
By better understanding the mechanisms involved in bacteria mutation and the development of superbugs, scientists can take a step toward finding effective solutions for antibiotic-resistant infections.
‘Survival gene’ stops strains of TB mutating into deadly ‘superbugs’ [news release]. University of Sussex’s website. . Accessed Jan. 30, 2017.