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

Gu, Jingang; Zhu, Chengliang; Cheng, Dazhi; Xie, Yan; Liu, Fang; Zhou, Xin

doi:10.1186/1476-511x-10-154

Cited by 23 publications

(18 citation statements)

References 27 publications

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“…Previous studies showed that HBV enhances apoM mRNA and protein expression, and that elevated levels of apoM suppress HBV protein expression and viral replication in HepG2 cells. However, these studies found no correlation between HBV viral load and apoM levels in patients with CHB [13]. Conversely, in this study, we found that higher HBV DNA levels were associated with higher serum apoM concentrations in patients with HBeAg-negative, but not HBeAg-positive, CHB.…”

Section: Discussioncontrasting

confidence: 88%

“…Similarly, HepG2 cells transfected with an infectious HBV clone were found to express significantly higher levels of apoM mRNA and protein than uninfected HepG2 cells in vitro. Moreover, apoM suppressed HBV replication in HepG2 cells [13]. However, the association between apoM expression and HBV replication rate in CHB patients is poorly understood.…”

Section: Introductionmentioning

confidence: 99%

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Positive association between serum apolipoprotein M levels and hepatitis B virus DNA load in HBeAg-negative chronic hepatitis B

Shen

et al. 2016

Lipids Health Dis

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BackgroundHepatitis virus B (HBV) has infected millions of people worldwide. Notably, such infections can be associated with hepatic complications. Levels of apolipoprotein M (apoM), a component of high-density lipoprotein (HDL), are known to be significantly elevated in patients with chronic hepatitis B (CHB). The aim of this study was to investigate the relationship between HBV DNA load in serum and serum apoM levels in patients with CHB.MethodsA total of 73 HBeAg-negative CHB patients, 50 HBeAg-positive CHB patients, and 79 non-CHB controls were included in the study cohort. The age and body mass index (BMI) of the study participants were matched. Serum levels of apoM and the HBV antigens HBsAg and HBeAg were measured by enzyme-linked immunosorbent assay (ELISA) analysis. Serum levels of alanine aminotransferase (ALT), aspartate transaminase (AST), cholesterol, and triglycerides (TG) were assessed using an automatic biochemical analyzer. Serum HBV DNA levels were quantified by real-time PCR analysis. Data were analyzed by Spearman’s rank correlation coefficient, Pearson correlation coefficient, and multivariate linear regression model (continuous variables), or Student’s t-test (mean differences).ResultsBoth the HBeAg-negative CHB and HBeAg-positive CHB patient groups exhibited elevated serum levels of apoM. Moreover, serum apoM levels were positively correlated with serum HBV DNA levels in HBeAg-negative CHB patients (r = 0.394, p < 0.001). Conversely, there was no significant relationship between apoM and HBV DNA levels in the HBeAg-positive CHB group (r = 0.197, p = 0.170). The median log copies/mL value for HBV DNA (4.00) was considered the cutoff point for the HBeAg-negative CHB group. Notably, a significant number of patients with HBV DNA levels above the cutoff point also had higher serum apoM levels (63.38 ± 29.84 vs. 41.41 ± 21.84; p = 0.001).ConclusionsOur findings reveal that the correlation between serum apoM levels and viral loads may depend on HBeAg status, as serum apoM levels were positively correlated with HBV DNA levels in HBeAg-negative CHB patients. These results suggest that HBeAg may play a role in apoM-related lipid metabolism and anti-inflammatory functions in hepatitis B patients. Thus, our findings may facilitate the clinical management of HBV infection.

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Section: Discussioncontrasting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Positive association between serum apolipoprotein M levels and hepatitis B virus DNA load in HBeAg-negative chronic hepatitis B

Shen

et al. 2016

Lipids Health Dis

View full text Add to dashboard Cite

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“…For example, serum high-density lipoprotein (HDL), low-density lipoprotein (LDL), total cholesterol (TC) and apolipoprotein B (ApoB) levels are decreased in hepatitis C virus-infected patients [ 15 – 17 ]. Our previous studies also found that HBV inhibited the synthesis and secretion of ApoB by inhibiting microsomal triglyceride transfer protein (MTP) expression [ 18 ], and the levels of serum ApoM was significantly elevated in patients as compared to healthy individuals, and enhanced ApoM levels in HBV infection may in turn suppress HBV replication [ 19 ]. Moreover, both Wang et al and Jiang et al confirmed that HBV inhibited the synthesis and secretion of ApoA1 in vivo and in vitro [ 20 , 21 ].…”

Section: Discussionmentioning

confidence: 99%

Hepatitis B virus inhibits apolipoprotein A5 expression through its core gene

Zhu

Gao²,

Song

et al. 2016

Lipids Health Dis

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BackgroundHepatitis B virus (HBV) infection causes lipid metabolism disorders. Apolipoprotein A5 (ApoA5) is a new apolipoprotein family member that plays an important role in the regulation of lipid metabolism. The present study was to investigate the impact of HBV on ApoA5 expression and its regulatory mechanism.MethodsReverse transcription polymerase chain reaction (RT-PCR) and western blotting were used to measure ApoA5 mRNA and protein expression in HepG2 and HepG2.2.15 cells. Enzyme-linked immunosorbent assay (ELISA) was used to measure the serum ApoA5 levels in healthy individuals and HBV patients. HBV infectious clone pHBV1.3 or individual plasmids expressing the HBV genome was cotransfected with the ApoA5 promoter pGL3-Apo5-LUC plasmid into HepG2 cells to assess the luciferase activity. RT-PCR and western blotting methods were used to detect Apo5 mRNA and protein expression, respectively.ResultsThe ApoA5 mRNA and protein expression levels were decreased in HepG2.2.15 cells compared with the control HepG2 cells. The serum ApoA5 levels were 196.4 ± 28.7 μg/L in the healthy individuals and 104.5 ± 18.3 μg/L in the HBV patients, statistical analysis showed that the ApoA5 levels were significantly lower in HBV patients than in the healthy individuals (P < 0.05). pHBV1.3 and its core gene inhibited ApoA5 promoter activity and mRNA and protein expression in HepG2 cells.ConclusionHBV inhibits ApoA5 expression at both the transcriptional and translational levels through its core gene.

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“…The APOM in serum of severe patients was downregulated compared with healthy and non-severe COVID-19 patients. Regulation of serum APOM has also been observed in hepatitis B virus (HBV) patients (Gu et al, 2011).…”

Section: Dysregulated Macrophage and Lipid Metabolismmentioning

confidence: 99%

Proteomic and Metabolomic Characterization of COVID-19 Patient Sera

Shen

Sun

et al. 2020

Preprint

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24Severe COVID-19 patients account for most of the mortality of this disease. 25 Early detection and effective treatment of severe patients remain major 26 challenges. Here, we performed proteomic and metabolomic profiling of sera 27 from 46 COVID-19 and 53 control individuals. We then trained a machine 28 learning model using proteomic and metabolomic measurements from a 29 training cohort of 18 non-severe and 13 severe patients. The model correctly 30 classified severe patients with an accuracy of 93.5%, and was further 31 validated using ten independent patients, seven of which were correctly 32 classified. We identified molecular changes in the sera of COVID-19 patients 33 implicating dysregulation of macrophage, platelet degranulation and 34 complement system pathways, and massive metabolic suppression. This 35 study shows that it is possible to predict progression to severe COVID-19 36 disease using serum protein and metabolite biomarkers. Our data also 37 uncovered molecular pathophysiology of COVID-19 with potential for 38 developing anti-viral therapies.

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

Cited by 23 publications

References 27 publications

Positive association between serum apolipoprotein M levels and hepatitis B virus DNA load in HBeAg-negative chronic hepatitis B

Positive association between serum apolipoprotein M levels and hepatitis B virus DNA load in HBeAg-negative chronic hepatitis B

Hepatitis B virus inhibits apolipoprotein A5 expression through its core gene

Proteomic and Metabolomic Characterization of COVID-19 Patient Sera

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