After studies of physics, James J. Collins obtained in 1990 his Ph.D. in Medical Engineering from the University of Oxford, with the support of a Rhodes Scholarship. Returning to the United States, he began in the Department of Biomedical Engineering at Boston University as a Research Assistant Professor, becoming a Professor in 1997.That same year, he co-founded the Center for BioDynamics of the university, which he continues to co-direct. In 2008 he became an Investigator of the Howard Hughes Medical Institute, and in 2010 a Visiting Professor in the Department of Systems Biology at Harvard Medical School. He is presently the William F. Warren Distinguished Professor at Boston University. His many honors include a MacArthur Fellowship and most recently membership in the American Academy of Arts & Sciences.
Prof. Collins discovered that major classes of bactericidal antibiotics, regardless of their drug-target interaction, induce a common oxidative damage cellular
death pathway. He showed that targeting bacterial systems that remediate oxidative damage is a viable means of potentiating bactericidal drugs and limiting the emergence of antibiotic resistance. He found that antibiotics can act as active, reactive mutagens, leading to multidrug resistance, a discovery with implications for the widespread use and misuse of antibiotics. He recently developed an inexpensive, clinically useful means for eradicating bacterial persisters, which are a sub-population of quasi-dormant cells that are resistant to antibiotic treatment. Prof. Collins’ work has important implications for reducing antibiotic resistance and establishing innovative new treatments for bacterial infections.
Professor John Mekalanos
After beginning his studies of bacteriology at the University of California, Los Angeles, where in 1978 he obtained his Ph.D. in microbiology, John Mekalanos pursued his postdoctoral research in the Department of Microbiology and Molecular Genetics of Harvard Medical School in Boston. His scientific career then developed in this department, as Assistant Professor in 1981, Professor in 1986 and Chairman in 1996. Currently he is the Adele H. Lehman Professor and Chairman of the department, now named Microbiology and Immunobiology. The recipient of many scientific awards, he was elected in 1997 to membership in the National Academy of Sciences (USA) and the American Academy of Microbiology.
Through his work on Vibrio cholerae and other bacterial pathogens, and his training of a new generation of scientists, Prof. Mekalanos has had a major impact on the field of bacterial pathogenesis. He has invented creative genetic and molecular approaches to identify the virulence factors and the complex mechanisms evolved by pathogens to regulate them. His research on cholera during the past 30 years has allowed us to understand how Vibrio cholerae causes this disease and how this organism has evolved. Moreover, his fundamental research has been effectively coupled with practical applications, leading to the development of both safe, effective vaccines and a novel small-molecule inhibitor of V. cholerae virulence, major advances for the prevention and treatment of this disease.
Professor Peter Palese
After receiving his doctorate in chemistry and a master’s degree in pharmacyat the University of Vienna, in Austria, Peter Palese joined in 1971 the Department of Microbiology of the Mount Sinai School of Medicine. He rose rapidly through the ranks, becoming Professor in 1978, Chairman in 1987, and was awarded a Dr. honoris causa in 2006. Among many honors, he was elected to membership in the National Academy of Sciences (USA) in 2000 and received the Robert Koch Prize in Berlin in 2006.
Prof. Palese has made a major contribution to our understanding of the influenza virus. He established the first genetic maps for the influenza A, B, and C viruses, identified the function of several genes of this virus, and defined the mechanism of neuraminidase inhibitors, which are now antiviral medicines approved by the Food and Drug Administration. He also pioneered the field of reverse genetics for negative strand RNA viruses, which allows the introduction of site-specific mutations into the genomes of these viruses. This revolutionary technique was crucial for the study of the functions of the viral genes and of viral pathogenesis, and facilitated the development of vaccines against the influenza virus. Reverse genetics also allowed Palese and colleagues to reconstruct and study the virus that caused the 1918 flu pandemic. Recently, Palese’s group in collaboration with Adolfo García-Sastre has developed approaches that should lead to a long-lasting universal influenza virus vaccine.
Professor Jeffrey V. Ravetch
After undergraduate training in molecular biophysics and biochemistry at Yale University, Jeffrey V. Ravetch entered the Rockefeller University – Cornell Medical School M.D./Ph.D. program, earning his Ph.D. in 1978 in genetics and his M.D. in 1979. Following postdoctoral studies at the National Institutes of Health, he joined the faculty of Memorial Sloan-Kettering Cancer Center and Cornell Medical College. In 1996 he was appointed Professor at the Rockefeller University, where he is now the Theresa and Eugene Lang Professor. Among many honors, he was elected to membership in the National Academy of Sciences (USA) in 2006 and received the Gairdner International Prize.
The studies carried out by Prof. Ravetch revealed the essential mechanisms by which antibodies mediate and regulate their diverse in vivo biological activities. His findings overturned dogma and revealed how antibodies can trigger inflammation, on the one hand, while suppressing inflammatory responses on the other, thereby resolving longstanding paradoxes on the contradictory nature of antibody function. These studies have fundamentally altered our understanding of this central class of immune mediators and have provided molecular explanations for their roles in host defence and vaccine design. New classes of therapeutic molecules for the treatment of infectious diseases have been developed as a result.