Precore/core region mutations of hepatitis B virus related to clinical severity

We studied the expression of the core region of the hepatitis B virus genome in mammalian cells with recombinant plasmid vectors. Stably transformed rat fibroblast cell lines were established by transfection with vectors containing subgenomic and genome-length hepatitis B virus DNA, followed by G418 selection. The RNA transcripts directed by the core region were characterized by Northern blot hybridization and S1 nuclease mapping. Using the chloramphenicol acetyltransferase gene expression system, the promoter activity located upstream of the core open reading frame was confirmed. The synthesis of core and e polypeptides was studied with a commercial radioimmunoassay. These studies show that partial deletion of the precore sequences abolished secretion of the e antigen, but there was pronounced synthesis of the core antigen in transfected cells.

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561 EFFECT OF ANTIVIRAL TREATMENTS IN EVOLUTION OF HEPATITIS B VIRUS (HBV) CORE REGION EPITOPES

Journal of Hepatology ◽

10.1016/s0168-8278(09)60563-8 ◽

2009 ◽

Vol 50 ◽

pp. S207

Author(s):

M. Homs ◽

R. Jardi ◽

M. Buti ◽

D. Tabernero ◽

P. Fernandez-Fernandez ◽

...

Keyword(s):

Hepatitis B Virus ◽

Hepatitis B ◽

Core Region ◽

B Virus

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Serum Clusterin: A Potential Marker for Assessing the Clinical Severity and Short-Term Prognosis of Hepatitis B Virus-Related Acute-on-Chronic Liver Failure

Disease Markers ◽

10.1155/2020/8814841 ◽

2020 ◽

Vol 2020 ◽

pp. 1-11

Author(s):

Huimin Liu ◽

Yuxin Li ◽

Fangyuan Gao ◽

Peipei Meng ◽

Hao Yu ◽

...

Keyword(s):

Hepatitis B Virus ◽

Hepatitis B ◽

Liver Failure ◽

Chronic Liver ◽

Clinical Severity ◽

Chronic Liver Failure ◽

Short Term ◽

Potential Biomarker ◽

B Virus ◽

Normal Controls

Background. Acute-on-chronic liver failure (ACLF) is a clinical syndrome characterized by acute deterioration of liver function and high short-term mortality. Clusterin, with biological functions similar to small heat shock proteins, can protect cells from apoptosis induced by various stressors. The aim of this study was to detect the level of serum clusterin in hepatitis B virus- (HBV-) related ACLF and to assess the predictive value of clusterin for the short-term prognosis of HBV-ACLF. Methods. We detected serum clusterin by ELISA in 108 HBV-ACLF patients, 63 HBV-non-ACLF patients, and 44 normal controls. Results. Serum clusterin was markedly lower in HBV-ACLF patients (median, 51.09 μg/mL) than in HBV-non-ACLF patients (median, 188.56 μg/mL) and normal controls (median, 213.45 μg/mL; all P < 0.05 ). Nonsurviving HBV-ACLF patients who died within 90 days had much lower clusterin levels than did surviving patients, especially those who died within 28 days (nonsurvival group vs. survival group: 39.82 ± 19.34 vs. 72.26 ± 43.52 , P < 0.001 ; survival time ≤ 28 vs. survival time > 28 : median 28.39 vs. 43.22, P = 0.013 ). The results showed that for identifying HBV-ACLF, the sensitivity of clusterin (93.7%) was similar to the sensitivities of the international normalized ratio (INR; 94.4%) and total bilirubin (TBIL; 94.8%), but its specificity (90.7%) was higher than that of prothrombin activity (PTA; 65.8%) and TBIL (69.8%) and was similar to INR (88.9%). As the concentration of clusterin increased, the mortality of HBV-ACLF patients decreased significantly from 59.3% to 7.0%. Clusterin had better ability for predicting the prognosis of HBV-ACLF patients than did the model for end-stage liver disease (MELD) score and the chronic liver failure consortium (CLIF-C) ACLF score (MELD vs. clusterin: P = 0.012 ; CLIF-C ACLF vs. clusterin: P = 0.031 ). Conclusion. Serum clusterin is a potential biomarker for HBV-ACLF which can be used to assess clinical severity and the short-term prognosis of patients with this disease and may help clinicians identify HBV-ACLF with greater specificity and improved prognostic accuracy than existing prognostic markers.

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