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. 2018 Feb 20:8:14.
doi: 10.1186/s13578-018-0215-5. eCollection 2018.

Correlation between hepatic human males absent on the first (hMOF) and viral persistence in chronic hepatitis B patients

Liwen Chen #  1 , Chuanwu Zhu #  2 , Fengdi Li #  1 , Yun Wang  1 , Rebecca Bao  3 , Zhujun Cao  1 , Xiaogang Xiang  1 , Lei Yan  1 , Lanyi Lin  1 , Gangde Zhao  4 , Qing Xie  1 , Shisan Bao  5 , Hui Wang  1
Affiliations

Correlation between hepatic human males absent on the first (hMOF) and viral persistence in chronic hepatitis B patients

Liwen Chen et al. Cell Biosci. .

Abstract

Background: Chronic hepatitis B (CHB) remains a global health dilemma with high morbidity and mortality. Human males absent on the first (hMOF) (a histone acetyltransferase) is responsible for DNA damage repair, tumorigenesis and cell cycle regulation. Persistence of HBV DNA contributes to cirrhosis and hepatocellular carcinoma (HCC) in CHB patients. Histone acetyltransferase enhances HBV replication, however the precise underlying mechanism of hMOF in HBV replication in CHB patients remains to be explored. This study aims to investigate the correlation between hepatic hMOF and HBV DNA replication in CHB patients, and may provide new insights towards the treatment of CHB patients.

Methods: hMOF in liver biopsy (CHB, n = 33 HBeAg+; n = 20 HBeAg-, and three healthy controls) was determined, using immunohistochemistry, qPCR and Western blot. The correlation between hMOF and HBsAg, as well as, HBeAg were determined.

Results: A positive correlation between hMOF and HBV DNA in overall CHB patients was observed. A distinct positive correlation between hMOF and HBsAg and/or HBeAg in HBeAg+ CHB patients was also detected, however not observed between hMOF and HBsAg in HBeAg- CHB patients. No correlation was observed between hMOF and hepatic inflammation severity and fibrotic stage in CHB patients.

Conclusions: Hepatic hMOF might contribute to host HBV clearance in CHB patients and possible pathogenesis.

Keywords: Chronicity; Epigenetic regulation; Hepatitis B; Viral replication; hMOF.

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Figures

Fig. 1
Fig. 1
Correlation between hepatic hMOF and serum HBV DNA, HBsAg, and HBeAg levels. Correlation between hepatic hMOF and serum HBV DNA, HBsAg and/or HBeAg levels in CHB patients (a, b), and HBeAg− CHB patients (c, d), and HBeAg+ CHB patients (e–g), and correlation between hepatic hMOF and combination of HBsAg–HBeAg in HBeAg+ CHB patients (h). Representative immunohistochemical micrographs of hepatic hMOF in different liver tissues: Healthy control (i); HBeAg− CHB patients with low HBV DNA load (j) and high HBV DNA load (k); HBeAg+ CHB patients with low HBV DNA load (l) and high HBV DNA load (m)
Fig. 2
Fig. 2
Hepatic hMOF in HBeAg+ and/or HBeAg− CHB patients and healthy controls. Hepatic hMOF production was presented with Western blot and quantitative analysis of hepatic hMOF mRNA expression was measured by qPCR, from HBeAg+ CHB patients (a) and HBeAg− CHB with high HBV DNA load (HBV DNA ≥ 105 IU/mL, 10 cases) and with low HBV DNA load (HBV DNA < 105 IU/mL, 10 cases), and healthy controls (HC) (three cases), and HBeAg− CHB (b) with high HBV DNA load (HBV DNA ≥ 104 IU/mL, 10 cases) and with low HBV DNA load (HBV DNA < 104 IU/mL, 10 cases), and healthy controls (HC) (three cases). The significant difference is expressed as *p < 0.05, **p < 0.01
Fig. 3
Fig. 3
Correlation between hepatic hMOF and severity of inflammation as well as, stage of fibrosis of liver. Correlations between hepatic hMOF and severity of inflammation and stage of fibrosis of liver was described in CHB patients (a, b), in HBeAg− CHB patients (c, d) and in HBeAg+ CHB patients (d, e)
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