Our major research interest is the origin, evolution and pathogenicity of HIV-1, the causative agent of AIDS. HIV-1 is the result of several zoonotic transmissions of simian immunodeficiency viruses (SIV) infecting chimpanzees or gorillas to humans. We found that only HIV-1 group M strains that account for >95% of infections worldwide are perfectly adapted to the human host and able to counteract or evade all immune defense mechanisms. We also like to clarify why monkeys that are naturally infected with SIV do usually not develop AIDS. It is known that high levels of chronic immune activation and programmed cell death drive progression to AIDS in humans. Our studies show that both viral properties and host factors help to explain why damaging hyper-activation of the immune system is observed in progressing HIV-1 infection but absent in asymptomatic naturally SIV-infected monkeys. Understanding the basis for the efficient spread of pandemic HIV-1 group M strains and the lack of disease progression in natural SIV infection may help to develop new preventive and therapeutic approaches.
Our second major research focus is the isolation, characterization and optimization of natural factors that modulate viral infections. By screening complex peptide-protein libraries from human sources, such as blood, semen, spleen, saliva and breast milk, we discovered several inhibitors of HIV-1 and other viral pathogens. This approach also allowed the identification of amyloid fibrils in semen that boost HIV-1 infection and might facilitate clearance of poor-quality sperm. Recently, we discovered a novel natural CXCR4 antagonist that not only blocks infection by CXCR4-tropic HIV-1 strains but also promotes the mobilization of stem cells and suppresses the migration of cancer cells. The discovery and optimization of further agents playing roles in infectious diseases and cancers is also an important goal of the recently established CRC 1279.