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Genital human papillomaviruses (HPVs) account for 99% of cervical cancers. Although vaccines against these HPV types are currently available, the exact mechanisms by which these viruses contribute to carcinogenesis are still not fully understood. In order to find preventive as well as therapeutic options, the relationships and interactions between the virus and the host cell must be clearly understood. In this context we are interested in the signal transduction pathways in which papillomaviruses interfere and how they change under certain conditions (e.g., after further infection with bacteria or under nutrient or oxygen deprivation).
Another focus is the relationship between “white” skin cancer and the infection with so-called cutaneous papilloma viruses. Although they are suspected – in conjunction with excessive sun exposure or under immune suppressive conditions – to promote the development of non-melanoma skin cancer, there are still no vaccines available. This is not least due to a lack of suitable preclinical model systems that reflect the situation in humans and in which such vaccines can be tested. In order to investigate these questions, suitable preclinical models are necessary. Only in this way other risk factors such as UV exposure and/or immunosuppression can be included and tested in the context of an entire organism.
The rodent Mastomys coucha represents such a model as it allows the analysis of basic mechanisms of papillomavirus-induced skin carcinogenesis. In this rodent that is infected with cutaneous papillomaviruses, the entire pathogenesis, starting from the first infection to the final development of skin tumors can be examined, both in immunologically and molecular biological terms. Here we have already developed a vaccine against papillomavirus-induced skin tumors which is completely protective even under immunosuppressive conditions. In addition, we are currently investigating how UV radiation in conjunction with a viral infection affects the genesis of skin tumors.