Biography of Kwang-Poo Chang (3-22-05)

K.-P. Chang graduated with B.Sc. from Department of Entomology, National Taiwan University. He subsequently received M.Sc. and Ph.D. in cell biology of insect endosymbiosis from Department of Biology, University of Guelph, Canada. From 1972 to 1983, he was Postdoctoral Fellow, Assistant and Associate Professor in Parasitology Laboratory of the late Professor William Trager, Rockefeller University. Since 1983, he has been Professor of Microbiology/Immunology, Chicago Medical School, University of Health Sciences (re-named recently as Rosalind Franklin University of Medicine and Science) (e-mail.Kwang-poo.chang@rosalindfranklin.edu).

His main research interest currently is to develop strategies of treatment and prevention of infectious and parasitic diseases through understanding molecular mechanisms of microbial virulence. Biological models studied include parasitic protozoa in mammalian cells and endosymbiotic bacteria in insects and protozoa. K.-P. Chang’s research has been supported previously by US-National Science Foundation, World Health organization and other funding sources. He has been supported continuously by US-NIH RO1 Grant No. AI-20486 since 1978 until now. The major focus of his research has been the molecular mechanisms of microbial virulence in Leishmania model. The key concept developed by studying this model is the proposal that there are three different groups of parasite molecules, which are involved in the progression of leishmaniasis from disease to cure. They include parasite molecules responsible for infection, for immunopathology as pathoantigens and for eliciting host immunity as “natural vaccines” (KP Chang, BS McGwire 2002 Kinetoplastid Biol. Dis. 1, 1-7; KP Chang et al. 2003 Acta Trop. 85, 375-90). Virulence factors of the pathogens include all molecules in these three functional sets as well as those relevant to drug-resistance. Independent up- and down-regulation of their expression in the parasites proves to affect their virulence in experimental models and predictably also the virulence of human diseases from asymptomatic infection to fatal cases. Virulence of human diseases is complicated by the necessity to consider additional risk factors in epidemiology, i. e. genetic, environmental and other conditions of the hosts (humans and reservoirs) and vectors in additional to those of the causative pathogens. It is advantageous to conceptualize infection-related molecules of pathogens, their pathoantigens and natural vaccines as independent, but indispensable elements in regulating microbial virulence, as they represent different functional targets for developing different strategies against microbial infection. The recent laboratory effort is to construct transgenic Leishmania for developing porphyria (Sah et al. 2002 J. Biol. Chem 277, 14902-9) in the hope that they can be exploited as inducible suicidal mutants to serve as a universal platform for effective delivery of natural and add-on vaccines against leishmaniasis and other infectious/parasitic diseases.