Discovery could transform Tb treatment

Dr Kiel Hards (foreground), watched by Prof Greg Cook, uses a chemostat in a laboratory at the University of Otago yesterday. Photo: Linda Robertson
Dr Kiel Hards (foreground), watched by Prof Greg Cook, uses a chemostat in a laboratory at the University of Otago yesterday. Photo: Linda Robertson
The ''holy grail'' for beating tuberculosis is a step closer thanks to the efforts of University of Otago researchers.

An international research team, which included Greg Cook and Kiel Hards from Otago University, found a ''chink in the armour'' of Tb that could lead to the development of a new generation of drugs to combat the deadly disease.

Prof Cook said the weakness they found had the potential to save and improve lives by making drug-resistant Tb more treatable and making treatment for other strains much faster.

After discovering the weakness, the researchers, with the help of $825,000 in Marsden funding, were now working on finding compounds that could take advantage of their discovery and lead to the creation of new drugs.

Prof Cook said it was a step towards the ''holy grail'' of being able to treat Tb in a matter of weeks rather than months or years.

''Our team is trying to develop new ways to treat this horrible disease, because our existing weapons against it are increasingly failing, too toxic and act too slowly.

''Finding new drugs is an incredibly difficult proposition, with only two new drugs licensed for Tb in decades.''

At the moment it took six months to treat non-drug-resistant strains of Tb and two years for the most drug-resistant forms.

It was also a major killer. The World Health Organisation says Tb is one of the top 10 causes of death worldwide and a leading killer of HIV-positive people. Globally, 1.8 million people died of the disease in 2015, and mortality rates were high for people who caught drug-resistant strains.

The weakness the researchers from Otago, Nanyang Technological University, Singapore, and Albert Einstein College of Medicine, United States found involved a protein that helped Tb breathe in oxygen.

The researchers developed a genetically modified form of Tb that did not have that protein.

When they did tests using mice, they found the modified form of Tb could be quickly cleared using existing drugs.

Now the researchers were looking for a compound that replicated the genetic modification and knocked out the protein.

''We do not yet know how it might work in humans, but this work clearly highlights the incredible potential of targeting the respiration of Tb with drugs that take out both respiratory oxidases.

''We think that it presents an excellent avenue to develop fast-acting drugs that synergise with current Tb medicines and could ultimately revolutionise the way we treat Tb infections.''


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