Published on January 21, 2014 at 12:25 AM
They found that when GAS adheres and infects the host's cells, it delivers into these cells two streptolysin toxins. These toxins impair the body's mechanism for quality control of protein synthesis. This in turn triggers a defensive stress response which, among other things, also increases the production of the amino acid asparagine. GAS senses the increased asparagine level and alters its gene expression profile — and its rate of proliferation, which can be deadly in the host.
The research team further discovered that asparaginase, a protein that digests asparagine and is a widely-used chemotherapeutic agent against leukemia, arrests GAS growth in human blood and in a mouse model of human bacterial infection. Asparginase has never before been used to treat GAS infections.
The findings of this study constitute a major advance of the concept that understanding the metabolic changes occurring between the pathogen and its host during infection can lead to development of new and more effective treatments against infectious diseases.
Yissum Research Development Company, the technology transfer arm of the Hebrew University, registered a patent for the discovery and is seeking commercial partners to help develop effective therapies against invasive streptococcus infections.