A novel compound that has the potential to starve the bacteria that causes tuberculosis – the world’s leading infectious killer after SARS-CoV2 – is entering human clinical trials.

A new method that analyzes how individual immune cells react to the bacteria that cause tuberculosis could pave the way for new vaccine strategies against this deadly disease, and provide insights into fighting other infectious diseases around the world.

Dr. David Russell, the William Kaplan Professor of Infection Biology in the Department of Microbiology and Immunology in the Cornell College of Veterinary Medicine, has used a cutting-edge method for illuminating the interaction between the bacteria that cause tuberculosis and two different kinds of host cells.

Cornell researchers have uncovered the structure of a regulatory mechanism unique to bacteria, opening the door for designing new antibiotics targeted to pathogens.

Brian VanderVen, assistant professor of microbiology and immunology, and colleagues at Cornell’s College of Veterinary Medicine, have discovered a key metabolic mechanism in Mycobacterium tuberculosis(Mtb) bacteria, which presents as a novel drug target for potentially treating tuberculosis. The finding is published in the journal eLife.

With a $1.5 million grant from the Bill & Melinda Gates Foundation, Cornell faculty have embarked on a quest to discover new drugs to combat tuberculosis (TB), the leading cause of death from bacterial infection. Because TB is an orphan disease –chiefly afflicting people in developing countries and offering poor profit prospects to most drug developers – this project is one of few to offer hope against an epidemic that grows more untreatable by the day.