Philipp Schult
Heidelberg University
11 Papers
28 Citations
Philipp Schult is an academic researcher from Heidelberg University. The author has contributed to research in topics: Viral replication & Hepatitis C virus. The author has an hindex of 7, co-authored 9 publications.
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Papers
microRNA-122 amplifies hepatitis C virus translation by shaping the structure of the internal ribosomal entry site
Philipp Schult,Hanna Roth,Rebecca L. Adams,Caroline Mas,Lionel Imbert,Christian Orlik,Alessia Ruggieri,Anna Marie Pyle,Anna Marie Pyle,Volker Lohmann +9 more
TL;DR: The authors show that microRNA-122 functions as an RNA chaperone that guides the formation of a functional internal ribosome entry site by preventing energetically more favorable secondary structures within the HCV RNA genome.
Tuning a cellular lipid kinase activity adapts hepatitis C virus to replication in cell culture.
Christian Harak,Max Meyrath,Inés Romero-Brey,Christian Schenk,Claire Gondeau,Philipp Schult,Katharina Esser-Nobis,Mohsan Saeed,Petra Neddermann,Paul Schnitzler,Daniel Gotthardt,Sofía Pérez-del-Pulgar,Christoph Neumann-Haefelin,Robert Thimme,Philip Meuleman,Florian W. R. Vondran,Raffaele De Francesco,Charles M. Rice,Ralf Bartenschlager,Volker Lohmann +19 more
TL;DR: This study has uncovered a long-sought mechanism of HCV cell-culture adaptation and demonstrates how a virus can adapt to changes in a cellular environment associated with tumorigenesis.
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Bile acids specifically increase hepatitis C virus RNA-replication.
Patrick Chhatwal,Dorothea Bankwitz,Juliane Gentzsch,Anne Frentzen,Philipp Schult,Volker Lohmann,Thomas Pietschmann +6 more
TL;DR: The increase of HCV replication by BAs may influence the efficacy of antiviral treatment in vivo and may improve replication of primary HCV genomes in cell culture.
Evidence for Internal Initiation of RNA Synthesis by the Hepatitis C Virus RNA-Dependent RNA Polymerase NS5B In Cellulo.
TL;DR: The data indicate that the HCV replicase is capable of internal initiation in its natural environment, although functional replication likely requires only terminal initiation.
5
DDX60L Is an Interferon-Stimulated Gene Product Restricting Hepatitis C Virus Replication in Cell Culture
Oliver Grünvogel,Katharina Esser-Nobis,Anna Reustle,Philipp Schult,Birthe Müller,Philippe Metz,Martin Trippler,Marc P. Windisch,Michael Frese,Marco Binder,Oliver T. Fackler,Ralf Bartenschlager,Alessia Ruggieri,Volker Lohmann +13 more
TL;DR: DDX60L knockdown did not alter interferon-stimulated gene (ISG) induction after IFN treatment but inhibited HCV replication upon ectopic expression, suggesting that it is a direct effector of the innate immune response.