Hepatocyte Factor JMJD5 Regulates Hepatitis B Virus Replication through Interaction with HBx

Journal of Virology
Takahisa KouwakiYoshiharu Matsuura

Abstract

Hepatitis B virus (HBV) is a causative agent for chronic liver diseases such as hepatitis, cirrhosis, and hepatocellular carcinoma (HCC). HBx protein encoded by the HBV genome plays crucial roles not only in pathogenesis but also in replication of HBV. Although HBx has been shown to bind to a number of host proteins, the molecular mechanisms by which HBx regulates HBV replication are largely unknown. In this study, we identified jumonji C-domain-containing 5 (JMJD5) as a novel binding partner of HBx interacting in the cytoplasm. DNA microarray analysis revealed that JMJD5-knockout (JMJD5KO) Huh7 cells exhibited a significant reduction in the expression of transcriptional factors involved in hepatocyte differentiation, such as HNF4A, CEBPA, and FOXA3. We found that hydroxylase activity of JMJD5 participates in the regulation of these transcriptional factors. Moreover, JMJD5KO Huh7 cells exhibited a severe reduction in HBV replication, and complementation of HBx expression failed to rescue replication of a mutant HBV deficient in HBx, suggesting that JMJD5 participates in HBV replication through an interaction with HBx. We also found that replacing Gly(135) with Glu in JMJD5 abrogates binding with HBx and replication of HBV. More...Continue Reading

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Citations

Nov 1, 2016·Expert Opinion on Drug Discovery·Liudi TangJu-Tao Guo
May 12, 2017·PLoS Pathogens·Chikako OnoYoshiharu Matsuura
Jun 25, 2017·Virus Research·Surya Agung PriyambadaKazuhito Fujiyama
Dec 22, 2020·Antiviral Research·Yuzy FauzyahYoshiharu Matsuura
Jan 13, 2021·Microbiology and Immunology·David Virya ChenToru Okamoto

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