Recent studies associate tuberculosis with a higher risk of various cancers. Tuberculosis causes chronic inflammation and scientists know that this can induce cancer. A new, effective treatment for tuberculosis may thus reduce the incidences of certain cancers in parts of the world where tuberculosis is common and hard to treat.

The team studying the toxin-antitoxin complex in tuberculosis bacteria relied on publicly available databases of molecular data to solve the structure of the complex. These included the Protein Databank (PDB) and the Universal Protein resource (UniProt). The researchers also used open-source software PyMOL to model the molecular structures.

Studies suggest that tuberculosis bacteria may have acquired the genes that code for the proteins to build the toxin-antitoxin complex by exchanging DNA with other bacteria. Horizontal exchange of DNA in this way is common amongst bacteria and enables them to evolve quickly. They are able to exchange lengths of DNA that confer resistance to drugs and so quickly evolve antibiotic resistance. The speed by which bacteria adapt to and thus bypass drugs is one reason why they are an increasing threat to human health worldwide.

Tuberculosis is one of the most widespread infectious diseases in the world with up to one third of the global population carrying the bacteria, although most don’t develop an active infection. Problems in effectively administering multi drug antibiotic treatments have been a factor in the development of tuberculosis bacteria that are resistant to a range of drugs. A new treatment therefore, based on a newly discovered molecular mechanism, will prove very valuable for human health. Other bacteria have toxin-antitoxin complexes so similar approaches could result in new, targeted antibiotics for other diseases.