Skip to main content

Secondary navigation:

Morrissey College of Arts and Sciences

Eva-Katharina Pauli

research assistant professor

Eva Pauli


Eva-Katharina Pauli

Ph.D., Center for Molecular Biology of Inflammation, Westfälische Wilhelms-Universität Münster, Germany


Fields of Interest

Virus-host interaction, signal transduction, intrinsic immunity, restriction factors

Academic Profile

Viral proteins or nucleic acids trigger signaling cascades resulting in high expression levels of antiviral restriction factors that eliminate the virus from the host. Viruses have evolved numerous strategies to inhibit or subvert this cellular response in order to ensure their replication. This interplay between host and virus resulted in a viral life cycle highly intertwined with many host cell functions.

My research focusses on regulation of cell signaling pathways during viral infection with the goal to elucidate novel mechanisms in the interplay between host and virus.

One research focus aims to define how viruses utilize cellular networks, such as the ubiquitin-proteasome-system. While the requirement of ubiquitinating enzymes for lentiviral replication is well established, the involvement of deubiquitinating enzymes is less well studied. With different molecular techniques such as overexpression/knock down we want to determine the relevance of deubiquitinases for the viral life cycle.

Another part of my work aims to uncover how viruses antagonize antiviral restriction factors to ensure their replication. A special focus lays on small viral proteins, also known as accessory proteins. These proteins are highly adapted to their specific hosts. They can function as direct antagonists of antiviral restriction factors and in addition, have the unique ability to interact with a diverse set of cellular proteins, thereby providing the virus with the necessary tools to change cellular pathways in favor of viral replication. With proteomic studies, e.g. Mass Spectrometry, I hope to define the interactome of such accessory protein. A major part of this work proteins from viruses as HIV, SIV, and Influenza A virus. 


Pauli EK, Chan YK, Davis ME, Gableske S, Wang MK, Feister KF, Gack MU.
The ubiquitin-specific protease USP15 promotes RIG-I-mediated antiviral signaling by deubiquitylating TRIM25.Sci Signal. 2014.

Haasbach E., Pauli EK, Spranger R. Mitzner D, Schubert U, Kircheis R. Planzo O. Antiviral activity of the proteasome inhibitor VL-01 against influenza A viruses. Antiviral Res. 2011

Dudek SE, Luig C, Pauli EK, Schubert U, Ludwig S. The clinically approved proteasome inhibitor PS-341 efficiently blocks influenza A virus and vesicular stomatitis virus propagation by establishing an antiviral state.J. Virol. 2010

Pauli EK, Schmolke M, Hofmann H, Ehrhardt C, Flory E, Münk C, Ludwig S. High level expression of the anti-retroviral protein APOBEC3G is induced by influenza A virus but does not confer antiviral activity. Retrovirology. 2009

Pauli EK, Schmolke M, Wolff T, Viemann D, Roth J, Bode JG, Ludwig S. Influenza A virus inhibits type I IFN signaling via NF-kappaB-dependent induction of SOCS-3 expression.PLoS Pathog. 2008

Bürckstümmer T, Kriegs M, Lupberger J, Pauli EK, Schmittel S, Hildt E. Raf-1 kinase associates with Hepatitis C virus NS5A and regulates viral replication.FEBS Lett. 2006