Author

Paul Rothhaar

Heidelberg UniversityORCID 0000-0002-9281-0371Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Research Focus:host-pathogen & immune response· 3 Research Focus:cell signaling & trafficking· 2 Organism:human· 2 Assay:proteomics· 2 Research Focus:protein folding & dynamics· 1 Approach:statistical model· 1

Frequent Co-Authors

Volker LohmanniD· 3 shared Colin ForsteriD· 2 shared Tomke Arand· 2 shared Andreas PichlmairiD· 1 shared Antonio PirasiD· 1 shared Carla E. Gallardo-Flores· 1 shared Che C. ColpittsiD· 1 shared Christian HeussiD· 1 shared

Activity by Year

2026-2026 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

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3 shared papersMicrobiology

Volker LohmannORCID

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3 papers

Recent·Most cited

Hepatitis C virus NS5A is not an effective antagonist of the canonical PKR-eIF2α pathway

Carla E. Gallardo-Flores, Lindsay L. Yu, Elana Kertzman, Paul Rothhaar, Volker Lohmann, Che C. Colpitts

This study shows that HCV NS5A does not inhibit the PKR-eIF2 pathway, contradicting previous claims and supporting that HCV replicates despite active PKR response.

bioRxiv · Oct 8, 2026 · PreprintMicrobiology

A novel dimerization site in non-structural protein 5A of hepatitis C virus regulates viral replication fitness

Paul Rothhaar, Thibault Tubiana, Colin Forster, Gabriel Vanegas Arias, Tomke Arand, Noemi Schäfer, Philipp Ralfs, Christian Heuss, Antonio Piras, Andreas Pichlmair, Xavier Hanoulle, Stéphane Bressanelli, Volker Lohmann

This study identifies a dimerization site in NS5A that enhances HCV replication fitness by promoting self-interaction, which inhibits NS3 and NS5B activity.

PLoS Pathogens · Aug 5, 2026Peer-reviewedMicrobiology

Hepatitis C virus replication fitness as a determinant of antiviral therapy outcome

Ha-Gyu Thomas Seong, Tomke Arand, Colin Forster, Micha Böhm, Eva Heger, John McLauchlan, Christoph Sarrazin, J Dietz, Rolf Kaiser, Volker Lohmann, Paul Rothhaar

This study examines how HCV replication fitness affects antiviral treatment outcomes, finding that high replication fitness can compensate for resistance mutations and contribute to DAA treatment failure.

bioRxiv · Feb 4, 2026 · PreprintMicrobiology