Kurzfassung

Viral entry into target cells is initiated by interactions between viral surface components and cell surface molecules. After interaction with the primary interaction partner, the virus is transferred to a secondary receptor complex yielding a large plasmalemmal entry platform for internalization. Key players on the cell surface include tetraspanins, heparan sulfate proteoglycans, integrins, growth factor receptors and glycolipids. Our results show that viral particles derived from the human...Viral entry into target cells is initiated by interactions between viral surface components and cell surface molecules. After interaction with the primary interaction partner, the virus is transferred to a secondary receptor complex yielding a large plasmalemmal entry platform for internalization. Key players on the cell surface include tetraspanins, heparan sulfate proteoglycans, integrins, growth factor receptors and glycolipids. Our results show that viral particles derived from the human papillomavirus type 16 trigger massive reorganisation of tetraspanins in the plasma membrane of different cell types, producing large plasmalemmal assemblies. Several questions yet remain open: Can stages be differentiated between initial virus contact and the final entry platform? What is the molecular architecture of these assemblies? How are viral platforms generated, by patching of preformed building blocks or by recruiting single molecules/small complexes to the viral binding site? Unravelling these questions, we will create a picture of virus induced supramolecular plasmalemmal assemblies. These are highly relevant issues both for the field of membrane micropatterning, as little is known about the nano-organisation of large plasma membrane assemblies, as well as for virology, as identifying novel components of the entry receptor complex and defining stages during viral platform formation will expand the molecular concept underlying viral infection.
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