Research Group Urs Greber


Oncolytic virus, DNA-tumor virus; Persistent infection, Hematopoietic stem cell transduction, Phenotypic variability of infection, Light microscopy, Anti-virals

Summary & Mission statement

Viruses have been associated with cancer in two ways –as cancer-causing viruses, and cancer-disruptingvectors. Regardless oftheir effects, all viruses have a dual nature. Particles are ‘passive substances’ lacking chemical energy transformation processes, whereas infected cells are ‘active substances’ turning-over energy, and causing disease. How virions (passive substances) convert to infected cells (active substances) has been a long-standing question in my laboratory.


How do viruses work,and how can virus vectors be best used in anti-cancer treatments? To address virus-cancer interactions, our research focusses on human adenoviruses, which infect a wide range of cell types. Infection outcome dependson innate and adaptive anti-viral immunity,and the viral use of host cell mechanisms. We engage forward genetics, system-wide analyses of proteins, lipids and nucleic acids, as well asstudies of molecules, organelles, cells and micro-tissue. Advanced light and electron microscopy, biochemical and cell biological tests, systems profiling and numerical models further enhance our analyse sof viral infection.We additionally have a strong interest in identifying chemical compounds with anti-viral activity, and elucidating their mode-of-action to stop natural infections, and safeguard against uncontrolled outbreak of replicating anti-cancer vectors. Further efforts of my laboratory explorehow viruses adapt to a dynamic host environment and to therapeutic pressure, which can occur in cancer therapy, for example. Our studies contribute to a better understanding of how viruses break down the defense barriers of the host. They provide a strong basis for clinical gene therapy, a field, which largely relies on viral vectors.


  • Adenoviral vector with shield and adapter increases tumor specificity and escapes liver and immune control. Schmid, M., Ernst, P.,Honegger, A., Suomalainen, M., Zimmermann, M., Braun, L., Stauffer, S., Thom, C., Dreier, B., Eibauer, M., Kipar, A., Vogel, V., Greber, U. F., Medalia, O. & Pluckthun, A. Nat Commun.2018, 9, 450.
  • Cycle-Dependent Kinase Cdk9 is a postexposure drug target against human adenoviruses. Prasad, V., Suomalainen, M., Hemmi, S. & Greber, U. F.Cell Acs Infect Dis2017, 3, 398-405.
  • Co-Option of membrane wounding enables virus penetration into cells. Luisoni, S., Suomalainen, M., Boucke, K., Tanner, L. B., Wenk, M. R., Guan, X. L., Grzybek, M., Coskun, U. & Greber, U. F. Cell Host Microbe2015, 18, 75-85.
  • Plaque2.0-A High-Throughput analysis framework to score virus-cell transmission and clonal cell expansion. Yakimovich, A., Andriasyan, V., Witte, R., Wang, I. H., Prasad, V., Suomalainen, M. & Greber, U. F. Plos One20148, 10, E0138760. 10.1371/Journal.Pone.0138760
  • Chemical induction of unfolded protein response enhances cancer cell killing through lytic virus infection. Prasad, V., Suomalainen, M., Pennauer, M., Yakimovich, A., Andriasyan, V., Hemmi, S. & Greber, U. F.J Virol. 2014, 88, 13086-98. 10.1128/Jvi.02156-14.
  • Tracking viral genomes in host cells at single-molecule resolution. Wang, I. H., Suomalainen, M., Andriasyan, V., Kilcher, S., Mercer, J., Neef, A., Luedtke, N. W. & Greber, U. F.Cell Host Microbe2013, 14, 468-80.