Prions and retroviruses -- an unholy...( In the Institute of Molecular Virolo...)

In the Institute of Molecular Virology of the GSF National Research Center for Environment and Health in Neuherberg/Munich (Helmholtz Association of German Research Centres) the group is continuing to search for cellular components whose make-up is changed as a result of a prion infection. In collaboration with colleagues from the Technical University of Munich and the University of Heidelberg, the group used micro-array technologies micro-arrays are chips with thousands or tens of thousands of DNA or protein probes - and could demonstrate that the expression of endogenous retroviruses is influenced by infectious prion proteins in tests with mouse cells.

Prions an abbreviation for proteinaceous infectious particles work as a trigger to a set of diseases of the brain and nervous system, the so-called spongiform encephalopathies. These include BSE in cattle, scrapie in sheep and Creutzfeldt Jakobs Disease in humans. Prions are structural variants of a normal protein found in healthy tissues especially in the brain. The devastating effect of infectious prions is that, once they have entered the organism, they can modify the normal "healthy" prion proteins to create more infectious prions, and thus cause the illness to progress. However, as yet, little is known about the molecular mechanisms of pathogenesis, the role of co-factors and the interaction of prion proteins with cellular components.

Retroviruses insert their genetic information into the genome of host cells. In the case of endogenous retroviruses, this involves retroviral infections from long ago, which were transmitted through many generations by means of the germ line. Nearly ten percent of the genome of mice and humans consists of endogenous retroviral sequences that have accumulated during the course of evolution. Indeed, most structural genes of endogenous retroviruses are inactive, but many regulatory elements, such as binding sites for transcription factors, often remain ac
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