New drug found to effectively fight latent TB

Washington, Sept 13: A new study by an Indian-origin scientist has shown that an investigative drug, called R207910, can effectively fight against latent bacteria that causes tuberculosis (TB).

R207910 is currently in clinical trials against multi-drug resistant tuberculosis strains, and scientists are hoping that it may now lead to improved and shortened treatments for this globally prevalent disease.

It is estimated that one third of the world population is infected, asymptomatically, with latent TB and is at risk of developing active TB disease during their life time.

In the new study, Anil Koul and colleagues at Johnson & Johnson, tested R207910 on dormant M. tuberculosis in three different laboratory models of latency. R207910 targets a protein (ATP synthase) essential for making cellular energy (ATP) in actively replicating TB.

According to the scientists, even dormant bacteria, which are usually physiologically "turned off", still need to produce small quantities of ATP to survive. Already, a block in ATP synthesis can be considered an Achilles heel for killing dormant bacteria.

This reasoning proved to be correct and R207190 could successfully destroy dormant bacteria by greater than 95 percent, while current drugs like isoniazid showed no effect.

To their surprise, they found that R207910 is slightly more effective in killing dormant bacteria as compared to actively replicating ones, a unique spin as all known TB drugs are more effective on replicating bugs.

Now, researchers hope to validate these results clinically, and note that ATP synthase should be looked at as a drug target for other persistent bacterial infections. (ANI)

Indian-origin researcher unveils gene behind debilitating lung disease

Washington, September 13: An Indian-origin researcher at the Johns Hopkins Bloomberg School of Public Health has unveiled a gene that acts as a "master switch" to turn on numerous antioxidant and pollutant-detoxifying genes to protect the lungs from environmental pollutants, such as cigarette smoke.

Associate Professor Shyam Biswal studied lung tissue samples from patients with chronic obstructive pulmonary disease (COPD), and found that expression of the regulating gene NRF2 was significantly decreased in smokers with advanced stage of the condition as compared to normal subjects.

Biswal previously identified that disruption of NRF2 expression in mice caused early onset and severe emphysema, which is a major component of COPD in human.

However, the status of this critical pathway in humans with COPD was unclear.

"This work clearly demonstrates that decline in our antioxidant system is involved in progression of COPD, which could also be the case for other environmental diseases. There is no treatment of COPD, but NRF2 could be a novel target for the development of new drug therapies," said Biswal.

Dr. Rubin Tuder, a University of Colorado expert who is a co-author of the study, said: "As we learn how the protective actions of NRF2 are decreased in the course of a lifetime of exposure to cigarette smoke, it opens new venues for the development of novel drugs fitted for individual patients in specific stages of the disease."

The study has been published in the American Journal of Respiratory and Critical Care Medicine. (ANI)