Mario Schelhaas

Research topic

Our laboratory studies the interactions that occur between incoming animal viruses and their host cells during early infection. Viruses are simple, obligatory, intracellular parasites that depend on the host cell for most of the steps in the replication cycle. This is particularly critical during cell entry, which occurs usually by endocytic uptake and intracellular vesicle transport to deliver the genome to the site of replication. For this, viruses hijack cellular processes for signaling, membrane trafficking, intra- and inter-cellular transport, nuclear import and export, and molecular sorting.  As such, viruses can also be used as valuable tools to analyze any cellular mechanism that they hijack. Accordingly, our research focusses as much on the understanding of the basic cell biology of of the cell as it does help to fight viral diseases.

Currently, we are interested in two complex cellular mechanisms that human papillomaviruses (HPV) hijack for their cell entry: (i) a novel endocytic mechanism that is barely understood, and that is in search for a cell biological function; (ii) mitosis and the cellular control of segregation of chromosomes. In this CRC, we ask how virus engagement of cellular receptor molecules regulates the novel endocytic pathway and how signals are translated into formation of endocytic pits using cellular and molecular techniques in combination with live cell and superresolution microsopy in live cells.

Publications

  • Aydin, I., and Schelhaas, M. (2016). Viral Genome Tethering to Host Cell Chromatin: Cause and Consequences. Traffic 17, 327-340.
  • Aydin, I., Villalonga-Planells, R., Greune, L., Bronnimann, M.P., Calton, C.M., Becker, M., Lai, K.Y., Campos, S.K., Schmidt, M.A., and Schelhaas, M. (2017). A central region in the minor capsid protein of papillomaviruses facilitates viral genome tethering and membrane penetration for mitotic nuclear entry. PLoS pathogens 13, e1006308.
  • Aydin, I., Weber, S., Snijder, B., Samperio Ventayol, P., Kuhbacher, A., Becker, M., Day, P.M., Schiller, J.T., Kann, M., Pelkmans, L., et al. (2014). Large scale RNAi reveals the requirement of nuclear envelope breakdown for nuclear import of human papillomaviruses. PLoS pathogens 10, e1004162.
  • Day, P.M., and Schelhaas, M. (2014). Concepts of papillomavirus entry into host cells. Current opinion in virology 4C, 24-31.
  • Mercer, J., Schelhaas, M., and Helenius, A. (2010). Virus entry by endocytosis. Annu Rev Biochem 79, 803-833.
  • Schelhaas, M., Ewers, H., Rajamaki, M.L., Day, P.M., Schiller, J.T., and Helenius, A. (2008). Human papillomavirus type 16 entry: retrograde cell surface transport along actin-rich protrusions. PLoS pathogens 4, e1000148.
  • Schelhaas, M., Malmstrom, J., Pelkmans, L., Haugstetter, J., Ellgaard, L., Grunewald, K., and Helenius, A. (2007). Simian Virus 40 depends on ER protein folding and quality control factors for entry into host cells. Cell 131, 516-529.
  • Schelhaas, M., Shah, B., Holzer, M., Blattmann, P., Kuhling, L., Day, P.M., Schiller, J.T., and Helenius, A. (2012). Entry of human papillomavirus type 16 by actin-dependent, clathrin- and lipid raft-independent endocytosis. PLoS pathogens 8, e1002657.
  • Spoden, G., Kuhling, L., Cordes, N., Frenzel, B., Sapp, M., Boller, K., Florin, L., and Schelhaas, M. (2013). Human papillomavirus types 16, 18, and 31 share similar endocytic requirements for entry. Journal of virology 87, 7765-7773.