Our main scientific interests are to better understand the interaction of hepatitis B virus (HBV) with its host and to develop new (gene and immune) therapeutic strategies to treat chronic viral hepatitis and hepatocellular carcinoma.
The majority of the team is currently focusing on how HBV is controlled by cellular defense mechanisms and by the systemic immune response, and how HBV manages to escape this immune control. To be able to study this, we have developed new animal and cell culture models of HBV infection and new molecular diagnostic assays. We have established two HBV-transgenic mouse lines as models for a vertical transmission, and have developed a mouse model of self-limited hepatitis B.
Based on an improved basic understanding of the control of HBV infection we are developing new treatment strategies to treat chronic viral hepatitis. For example, we study the molecular mechanisms of antiviral effects of cytokines and other immune mediators, and investigate the possibility of a therapeutic cytokine gene transfer. Since we are convinced that immune tolerance needs to be overcome to cure chronic infection, we also follow strategies of therapeutic vaccination and try to redirect T cells to infected cells by generating recombinant T cell receptors. By grafting them onto primary T cells we follow a novel strategy in the treatment of infectious diseases.
Other topics of our group are metabolic alterations caused by hepatitis C virus, T cell therapy of HCV and hepatocellular cacinoma and developing new vectors systems for a liver directed gene transfer. As the first group worldwide, we managed to generate HBV based viral vectors. Recently, we successfully used HBV based vectors in a preclinical study in HCV infected chimpanzees.

Selected publications:

Hösel M, Quasdorff M, Webb D, Zedler U, Esser K, Arzberger S, Wiegmann K, Kirschning CJ, Langenkamp A, Rose-John S and Protzer U. Not interferon, but IL-6 controls early gene expression in Hepatitis B virus (HBV) infection. Hepatology 2009, 50:1773-1782.

Bohne F, Chmielewski M, Ebert G, Wiegmann K, Kürschner T, Schulze A, Urban S, Krönke M, Abken H, Protzer U. T cells Redirected Against Hepatitis B Virus Surface Proteins Eliminate Infected Hepatocytes. Gastroenterology 2008, 134: 239-47.

Quasdorff M, Hösel M, Odenthal M, Zedler U, Bohne F, Gripon P, Dienes HP, Stippel D, Goeser T, Protzer U. A concerted action of HNF1 a and HNF4a links hepatitis B virus replication to hepatocyte differentiation. Cellular Micobiology 2008, 10:1478-1490.

Protzer U, Seyfried S, Quasdorff M, Sass G, Svorcova M, Webb D, Bohne F, Hösel M, Schirmacher P, Tiegs G.
Antiviral activity and hepatoprotection by heme oxygenase-1 in hepatitis B virus infection. Gastroenterology 2007, 133: 1156-65.

Untergasser A, Zedler U, Langenkamp A, Hösel M, Quasdorff M, Esser K, Tapperzhofen B, Kolanus W and Protzer U. Dendritic cells take up viral antigens but do not support the early steps of hepatitis B virus infection. Hepatology 2006, 43: 539-547.

Untergasser A & Protzer U. Hepatitis B virus vectors allow elimination of viral gene expression and insertion of foreign promoters. Human Gene Therapy 2004, 15: 203-210.

Sprinzl M, Oberwinkler H, Schaller H, Protzer U.
Hepatitis B virus genome transfer with adenoviral vectors into cultured cells and mice: crossing the species barrier Journal of Virology 2001, 75: 5108-5118.

U. Klöcker, U. Schultz, H. Schaller, U. Protzer.
Liver macrophages release mediators after endotoxin stimulation that inhibit an early step in hepadnavirus replication. Journal of Virology 2000, 74 (12): 5525-5533.

Protzer U, Nassal M, Chiang PW, Kirschfink M, Schaller H. Interferon gene transfer by a novel hepatitis B virus vector efficiently suppresses wildtype-virus infection. PNAS 1999, 96: 10818-10823.

https://web.med.tum.de/virologie/home/