Enchanced levels of apolipoprotein M during HBV infection feedback suppresses HBV replication

Lipids in Health and Disease

Xin Zhou³  Fang Liu⁴  Yan Xie³  Duo-zhi Cheng²  Cheng-liang Zhu¹  Jin-Gang Gu³ 

[1] Department of Clinical Laboratory, Renmin Hospital of Wuhan University, Wuhan, Wuhan 430060, P.R. China;Department of Clinical Laboratory of Taihe Hospital Affiliated to Hubei Medical College, Shiyan, 442000, P.R. China;Center for Gene Diagnosis, Zhongnan Hospital, Wuhan University, Wuhan, 430071, P.R. China;The State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, P.R. China

关键词: Replication;    RT-PCR;    ELISA;    Apolipoprotein M;    Hepatitis B virus;   

Others  :  1212528
DOI  :  10.1186/1476-511X-10-154

 received in 2010-10-31, accepted in 2011-08-29,  发布年份 2011

【 摘 要 】

Background

Chronic liver diseases can interfere with hepatic metabolism of lipoproteins, apolipoproteins. Hepatitis B virus (HBV) is a major etiological agent causing acute and chronic liver diseases. Apolipoprotein M (ApoM) is a high-density lipoprotein (HDL) apolipoprotein and exclusively expressed in the liver parenchyma cells and in the tubular cells of the kidney. This study was to determine the correlation between HBV infection and ApoM expression.

Materials and methods

Serum ApoM levels in patients with HBV infection and in healthy individuals were measured by ELISA, ApoM mRNA expression were determined by RT-PCR, and the expression of S and E proteins of HBV, as well as the synthesis of viral DNA were measured by ELISA and real-time PCR.

Results

The levels of serum ApoM was significantly elevated in patients as compared to healthy individuals (P < 0.001), ApoM promoter activity, mRNA and protein expression were all stimulated in cells transfected with infectious HBV clone. In addition, ApoM decreases the expression of S and E proteins of HBV and the synthesis of viral DNA.

Conclusion

Raised ApoM levels in HBV infection may in turn suppress HBV replication, one of the protective mechanisms of nature.

【 授权许可】

   
2011 Gu et al; licensee BioMed Central Ltd.

【 图 表 】

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