Main Projects

  1. Chronic pulmonary infection of mice with MHV-68 as a model to study progressive pulmonary fibrosis. We use the MHV-68 infection of mice to study the role of chronic gammaherpesvirus infection in the pathophysiology of idiopathic pulmonary fibrosis (IPF). Specifically, we i) study the role of chronic gammaherpesvirus infection in the pathophysiology of IPF, ii) determine molecular mechanisms involved in disrepair of the injured lung and iii) test and define novel therapeutic strategies.
  2. Nanoparticles and persistent virus infection - a dangerous liaison for the development of chronic lung disease(s)? We investigate the interaction between nanoparticle exposure and persistent virus infection. Inhalation of environmental (nano)particles (NP) is known to trigger adverse reactions in the respiratory system, e.g. increased rates of chronic pulmonary diseases like COPD exacerbations for traffic emissions, or even cancer and fibrosis for respirable fibers. Several studies imply that herpesvirus infection may contribute to the development of pulmonary fibrosis. Since every human being is persistently infected with herpesviruses, we propose that the combination of NP exposure and persistent virus infection may result in chronic lung disease. Therefore, we want to investigate whether the interaction between NP and virus infection leads to more severe disease than exposure to each factor alone. We will determine the underlying molecular mechanisms and subsequently try to develop novel therapeutic strategies. This project is accomplished in close cooperation with the laboratories of T. Stoeger and P. Schmitt-Kopplin.
  3. Assessment of the role of various gammaherpesvirus genes in virus-host interaction and pathogenesis. We investigate the role of genes specific for MHV-68, of MHV-68 genes encoding cellular homologs, and of MHV-68 genes which are homologous to KSHV and/or EBV. The studies are based on a BAC-cloned MHV-68. The BAC technology is applied to genetically manipulate the MHV-68 genome by generating deletion mutants, inserting genes from KSHV or EBV, or replacing MHV-68 genes by homologous genes derived from EBV or KSHV. We focus on latency associated genes and potential oncogenes.