Academic Affiliation
Professor, School of Life Sciences in the College of Liberal Arts and Sciences
Credentials
PhD, 1974, Medical College of Georgia
Bio
A scourge to humankind throughout recorded history, tuberculosis (TB) continues to have a devastating impact even today. The World Health Organization has estimated that one-third of the world’s population is infected with Mycobacterium tuberculosis, with approximately 8 million new cases diagnosed annually. Although not everyone who is infected develops active disease, of those who do, nearly two million die each year. The severity of this global epidemic is exacerbated by the concomitant epidemic of HIV infection and the synergistic effect of the two diseases has profound economic implications, as well as untold human suffering.
Understanding the mechanisms by which M. tuberculosis causes TB is the overall goal of research conducted in the Clark-Curtiss laboratory. M. tuberculosis is transmitted from infected humans to non-infected ones via nasal droplets. After the bacteria are introduced into the lungs, they are ingested by macrophages, whose normal function is to destroy invading pathogenic microorganisms. M. tuberculosis has developed means to thwart normal macrophage function, and the bacteria are able to survive and grow within the phagosomal compartment. Development of TB disease occurs in individuals whose immune systems fail to recognize the presence of the bacteria and destroy them. Research in my lab has been directed toward understanding the genes and gene products of M. tuberculosis that are important to the intracellular survival and growth of the bacteria when they are in human macrophages. Areas of research that are currently being pursued: (a) identification and characterization of genes from M. tuberculosis that are differentially expressed by the bacilli when they are actively growing within human macrophages, using the selective capture of transcribed sequences (SCOTS) technique developed in my lab; (b) analysis of the regulation of mycobacterial gene expression in response to the environment of the human macrophage phagosome; and (c) mutagenesis of specific genes identified in (a) and (b) and analysis of the effects of such mutations on the ability of M. tuberculosis to survive in human macrophages and in animal infection models.