Research Group EBV Genetics and Vectors

Objectives

We are interested in Epstein-Barr virus (EBV). It is an important infectious agent and human pathogen but also provides several fascinating models that are accessible and can be studied in the laboratory. These models are relevant because some reflect fundamental aspects of herpes virus biology or shed light on the development of certain disease linked with EBV:

  • EBV is a paradigm of herpesviral latency because this virus establishes a stable latent infection in human cells in vitro.
  • EBV provides a tractable tumor model because it can induce proliferation of primary resting B cells, which become immortalized (and latently infected) upon infection with EBV.
  • EBV can escape from latency, which is another attractive model of herpes virus biology. This model is amenable to study in vitro, which is a rare exception in the field of viruses in general.
  • EBV is an interesting paradigm of a gene vector because it can stably deliver viral genes or, alternatively, other genes (or antigens) of interest to human cells.

Studying certain aspects of EBV’s biology can be problematic, which led us to develop new tools and approaches as needed. One of these problems was EBV’s genetic information, its DNA, which could not be manipulated in vitro in the past. We have developed techniques, which now permit the unrestricted genetic analysis of any viral gene in the context of EBV’s genome supporting our research and the research community worldwide. Our universal genetic approach has been a major investment, which now also strengthens one of our long-term visions of developing a safe and efficient EBV vaccine.

In our research we try to identify and address those questions, which are central to EBV’s life style, EBV’s biology and EBV-related diseases. For example, we wish to know how EBV induces proliferation of primary resting B cells. Several viral gene products contribute to this complicated process but not all their functions are known. In studying these viral genes we learn about paradigmatic concepts of cell transformation that this virus induces, a hallmark of tumorigenesis. A second example concerns the reactivation of herpes viruses from latency. Here, we are interested in the interplay between the virus and its cellular host. We focus on this relationship, which appears harmonious and almost symbiotic during herpesviral latency. How the virus escapes from latency, gains control of its gene expression and governs the cellular machinery is a third example of our scientific interests.

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