Current liver research: Hepatitis B virus alters lipid metabolism of host cells
7 July 2014
Chronic hepatitis B virus (HBV) infection has been associated with alterations in lipid metabolism. However, still little is known about how the pathogen exactly influences hepatocyte function. Scientists led by Prof. Maura Dandri and Prof. Jörg Heeren now demonstrated new findings: Using a human liver-chimeric mouse model, they could show how HBV infection altered metabolic gene expression. Most notably, the expression of CYP7A1, a key enzyme involved in bile acid synthesis, is significantly increased. Moreover, the data indicate that it is the binding of the virus to the host cell surface that causes these alterations. Viral particles bind to and suppress the activity of the receptor and bile acid transporter NTCP. 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. For the SFB scientists, these findings underline the importance to further exploit NTCP-related viral-drug interactions: NTCP is also involved in drug uptake. 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 Apr 8. doi: 10.1002/hep.27159. [Epub ahead of print]
For further information on Prof. Maura Dandri’s SFB project A5 “Molecular mechanisms of hepatitis B virus persistence in chronically infected uPA chimera mice” click here.
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” click here.