Giuseppe Legname completed undergraduate and postgraduate studies in biochemistry and molecular biology at the Università degli Studi of Milan, Italy. In 1997 he received his Doctor of Philosophy degree in Biological Sciences from the University of Warwick, Coventry, England, under the supervision of Professor J.M. Lord. After a long spell in Industry (Italfarmaco S.p.A.) where he co-authored many scientific papers and patents in the field of immunotherapy, he moved to academia at the National Institute for Medical Research (NIMR), Medical Research Council in Mill Hill, London, England. During the three years at NIMR, his research focused on the study of the signal transduction mechanisms and molecular requirements for thymocyte development and differentiation. The results of this work were published in the journal Immunity. As a follow-up of this research, he was able to make additional observations on T lymphocytes survival. These novel findings were published in the journal Science.
In 1999 he joined the faculty of the Department of Neurology at the University of California at San Francisco (UCSF), California, USA. During the seven-and-a-half years at UCSF he was involved in basic research projects in the field of Prion Biology and Disease at the Institute for Neurodegenerative Diseases (IND), under the direction of 1997 Nobel Laureate Professor Stanley B. Prusiner. During his stay at IND-UCSF, Giuseppe Legname co-authored many seminal papers in the field of Prion Biology and Disease, among others the first report on the making of synthetic prions, published in the journal Science.
Since December 2006, he has joined the faculty of the Scuola Internazionale Superiore di Studi Avanzati (SISSA), in Trieste, where he is currently managing a new Prion Biology Laboratory. The main focus of his research program is in the field of mammalian Prion Biology (physiological function of the prion protein in mammals) and Prion Disease (mechanisms of prion replication and structural characterization of molecular determinants for prion infectivity).