In collaboration with the Helmholtz Center Munich (EKLiP) and the Department of Infectious and Tropical Medicine, a biobank and observational study with 250 participants infected with the attenuated yellow fever vaccine virus YF-17D was established. The study aims to investigate the influence of genetic and non-genetic factors on an antiviral immune response, to identify early predictors for the strength of the individual adaptive immune response, and to find out what makes this vaccine, empirically developed in 1930, so potent. In cooperation with the working groups of Dr. Kai Dallmeier at the Rega Institute in Leuven, and Dr. Beate Kümmerer at the University of Bonn, three new fluorescence-based assays were developed to test the activity of neutralizing antibodies in sera against the yellow fever vaccine virus and other flaviviruses. These allow for a significant simplification and acceleration of measurement compared to previously established methods. Together with Dr. Giovanna Barba-Spaeth at the Institut Pasteur in Paris, it was shown that pre-existing vaccination against the TBE virus followed by vaccination against the yellow fever virus induces large amounts of non-neutralizing antibodies that cross-react with a variety of flaviviruses and through the phenomenon of "antibody-dependent enhancement" (ADE), can increase the risk of a severe course in case of infection with the dengue or Zika virus.
In collaboration with Prof. A. Krug from the Institute of Immunology and Dr. C. Geldermacher from the Department of Infectious and Tropical Medicine, the differences and similarities in the activation profiles of antigen-presenting cells from patients with mild SARS-Cov2 infection and participants after yellow fever vaccination were elucidated.
In a case of a patient with agammaglobulinemia and the flare-up of a chronic uncontrollable rubella infection many years after the presumed primary infection, it was shown that escape mutations of the virus in immunodominant peptides for the patient-specific HLA type, as well as the development of an exhausted T-cell phenotype in the patient, were responsible for the loss of virus control with ultimately fatal outcome.
