Innate Immunity and Viral Evasion

If a virus attacks us, our immune system registers this attack and starts a whole chain of reactions. Messengers initiate the release of cellular proteins, through which our cells prevent the spread of viruses – known as antiviral factors. However, some viruses have developed very effective strategies against these antiviral factors, so that the self-protection mechanism of the cells is ultimately insufficient to defend against the infection. Wanted: new antiviral factors which can fight off even these viruses – of which HIV is one. 


Our Research

The research group "Innate Immunity and Viral Evasion" is interested in gaining a better understanding of the interplay between host cells and viruses at the cellular and molecular level. HIV-1, the causative agent of AIDS, remains one of the most devastating viral pathogens worldwide and causes chronic immunodeficiency. Using human target cells of HIV-1, we characterize their ability to sense, with the help of the cellular pattern recognition receptors, an invading HIV-1 infection, and how efficiently this information is translated into a functional antiviral state. Vice versa, we identify and elucidate HIV-1-mediated evasion strategies of this cellular innate immunity, which explain why HIV-1 is successfully circumventing cellular defense mechanisms. Furthermore, we investigate the mode of action of cellular restriction factors, focusing on the antiviral proteins 90K and SERINC5, which can reduce the infectivity of HIV-1 particles.

Knowledge on these naturally occurring molecular weapons of human cells, and how HIV-1 has evolved to counteract them, could pave new avenues towards antiviral drugs.  In addition, together with our cooperation partners from Hannover Medical School, we are developing strategies for eradication of latently HIV-1-infected resting T-cells.

The research group "Innate Immunity and Viral Evasion" is also investigating the entry process of Chikungunya viruses. Chikungunya virus is an emerging and rapidly expanding pathogen which causes, in most of the cases, acute infections. A subset of infected persons, however, suffers from chronic joint pain and inflammation, justifying research to develop protective and/or therapeutic options which are completely missing to date. Using lentiviral pseudotypes carrying the CHIKV glycoproteins, we study means to inhibit entry of CHIKV into host cells using immunological and pharmacological approaches.

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