Modulation of microbial communities in virus infected hosts
We use animal models to determine viral and host factors that influence bacterial super infections.
Viruses highly depend on their hosts to replicate. Thus, they shape their environment to gain optimal conditions for replication. At the same time the host developed mechanisms to counteract the virus by means of its innate and adaptive immune system. This so called "molecular arms race" results in fascinatingly complex interaction networks.
But viruses not only interact with their host, they also change replication condition for other microbes in their direct and distant environment. This changes composition of commensal (“healthy”) microbes and lays ground for invasion of bacterial pathogens. Bacterial super infections pose a serious problem in public health and the underlying molecular mechanisms are still matter of debate. Using influenza A virus in established mouse models we are investigating the triangular relationship of virus, host and bacteria.
In a second branch of research we focus on immune-modulatory RNAs, which we are aiming to use as novel vaccine platforms. Systematic vaccination against infectious diseases was probably the main contribution to extension of life expectancy and increase of life quality since the late 18th century. Successful vaccines led to eradication of smallpox virus and quasi eradication of polio, being now endemic in only three countries worldwide. However, against other globally relevant diseases like HIV successful vaccine strategies are still missing or require continuous annual revaccination, as in case of influenza A viruses. New vaccine platforms are urgently needed to develop alternative strategies.