Outstanding publication: UKE award for CRC 841 doctoral student
8 December 2015
Nicola Oehler was awarded this year’s “Outstanding paper with student first authorship” prize by the Faculty of Medicine, University of Hamburg for her publication “Binding of hepatitis B virus to its cellular receptor expression profiles of genes the age of bile acid metabolism” (Hepatology, 2014). Her medical PhD thesis is jointly supervised by the CRC 841 project leaders Prof. Dr. Maura Dandri (A5) and Prof. Dr. Joerg Heeren (B6).
The study investigates the influence of the hepatitis B virus (HBV) on lipid metabolism of infected liver cells. It is the binding of the virus to the host cell surface that causes alterations: Viral particles bind to and suppress the activity of the receptor and bile acid transporter NTCP. Using a human liver-chimeric mouse model, Oehler and colleagues could demonstrate a possible consequence: the cell reacts to decreased NTCP function with adjustments in expression of metabolic genes, in order to maintain intracellular cholesterol and bile acid homeostasis. Most notably, the expression of CYP7A1, a key enzyme involved in bile acid synthesis, is significantly increased. These findings underline the importance to further exploit NTCP-related viral-drug interactions. NTCP is also involved in drug uptake and as HBV suppresses the activity of the transporter, the efficacy of certain drugs could be reduced in HBV-infected patients.
Oehler N, Volz T, Bhadra OD, Kah J, Allweiss L, Giersch K, Bierwolf J, Riecken K, Pollok JM, Lohse AW, Fehse B, Petersen J, Urban S, Lütgehetmann M, Heeren J, Dandri M
Binding of hepatitis B virus to its cellular receptor alters the expression profile of genes of the bile acid metabolism
Hepatology. 2014 Nov;60(5):1483-93. doi: 10.1002/hep.27159. Epub 2014 May 19.
For further information on Prof. Maura Dandri’s SFB project A5: Molecular mechanisms of hepatitis B virus persistence in chronically infected uPA chimera mice.
For further information on Prof. Jörg Heeren‘s SFB project B6: Development and progression of NASH and metabolic liver inflammation: the role of TREM-2.