Institute for Medical Virology and Epidemiology of Viral Diseases

A major effort of the lab is to clarify the causes and consequences of HIV induced generalized immune activation. HIV-1 can infect resting T cells but needs to drive cellular activation for efficient viral gene expression and thus completion of the viral life cycle. Hence, a concept of HIV/AIDS pathogenesis is that this immune activation results in increased T cell hyperproliferation and turnover. Ultimately, continuous T cell death leads to an exhaustion of the regenerative capacity of the immune system, loss of total T cell numbers and therefore AIDS. We analyze the mechanisms by which HIV proteins induce unspecific immune activation and thereby generate a cellular environment promoting viral replication. On the other hand, we investigate how the virus manages to evade the specific antiviral innate and adaptive immune response of the host and counteracts cellular restriction factors.

Another cell biology focused project is the release route of Hepatitis C Virus. Viruses hijack cellular pathways in order to produce infectious viral progeny. Elusive up to now, we have shown that HCV is not released via classical Golgi-mediated secretion. In contrast, HCV bypasses this cellular organelle and uses a pathway directly from the endoplasmic reticulum to the plasma membrane. This exciting results point towards the possible existence of a not yet described cellular secretion route, which could represent a seminal cell biological finding. We aim to identify host cell factors involved in this pathway and use HCV as a molecular tool.

Our basic research converges with therapeutic applications and culminated in the initiation of various projects with the aim to develop and establish novel antivirals. Examples are targeting of HIV-1 infected cells by immunotherapeutic antibodies, a small compound with a broad antiviral activity against Flaviviruses, small-peptide inhibitors of herpesvirus entry, as well as the potential utilization of virosomes as vaccines.