Changes in human behaviors are known factors favoring the emergence, reemergence, and rapid spread of infectious disease, such as prion diseases. The BSE crisis in the 1980 in Great Britain has likely been caused by decreasing inactivation of the BSE Prion during animal by-product processing, and an increased use of ruminant tissue proteins in farmed animal nutrition. This resulted in an explosive amplification of BSE-Prions in British cows, and eventually lead to numerous human BSE cases.

Even after decades of research, the molecular mechanism of prion spread and amplification is essentially not understood. At the same time, prion diseases do still occur in animals that serve as human food sources. Of particular concern is the spread of Cronic Wasting Disease in wild deer. But also the BSE thread has far from vanished. In order to fully understand the risks for humans, it is necessary to know all susceptible species, and understand the molecular mechanisms that lead to prion adaptation to new host species. Thus, one of our main research focuses is on the molecular mechanism of prion strain-barriers, and interspecies transmission barriers.