Developmental regulation of hepatitis B virus biosynthesis by hepatocyte nuclear factor 4alpha.

Abstract

The host cellular factors that promote persistent viral infections in vivo are, in general, poorly understood. Utilizing the hepatitis B virus (HBV) transgenic mouse model of chronic infection, we demonstrate that the nuclear receptor, hepatocyte nuclear factor 4alpha (HNF4alpha, NR2A1), is essential for viral biosynthesis in the liver. The dependency of HBV transcription on HNF4alpha links viral biosynthesis and persistence to a developmentally regulated transcription factor essential for host viability.