Hepatitis B virus mutations associated with in situ expression of hepatitis B core antigen, viral load and prognosis in chronic hepatitis B patients

2008 ◽  
Vol 204 (10) ◽  
pp. 731-742 ◽  
Author(s):  
Rong Zhu ◽  
Hui-Ping Zhang ◽  
Hui Yu ◽  
Hua Li ◽  
Yu-Qin Ling ◽  
...  
Author(s):  
Zhan-qing Zhang ◽  
Bi-sheng Shi ◽  
Wei Lu ◽  
Dan-ping Liu ◽  
Dan Huang ◽  
...  

Background. Changes of hepatitis B core antigen antibody (anti-HBc) in liver pathological involvement in patients with chronic hepatitis B virus (HBV) infection have not been investigated in detail. This study aimed to explore evolving patterns of anti-HBc following liver pathological states and to investigate validities of anti-HBc for predicting liver pathological states. Methods. 254 HBeAg-positive and 237 HBeAg-negative patients with chronic HBV infection were enrolled. Liver pathological diagnoses referred to Scheuer standard, and anti-HBc was measured using chemiluminescence microparticle immunoassay. Results. Anti-HBc was significantly positively correlated with pathological grades and stages in both HBeAg-positive (rs = 0.312, P<0.0001, and rs = 0.268, P<0.0001) and HBeAg-negative (rs = 0.270, P<0.0001, and rs = 0.147, P=0.0237) patients. The medians of anti-HBc in pathological grades of G1, G2, and G3 and stages of S1, S2, S3, and S4 in HBeAg-positive patients were all significantly lower than those in HBeAg-negative patients (all P<0.005). The areas under receiver-operating characteristic curves (95% confidence interval) of anti-HBc for predicting pathological grades ≥G2 and ≥G3, and stages ≥S2 and =S4 in HBeAg-positive patients were 0.683 (0.622–0.740) and 0.662 (0.601–0.720), and 0.627 (0.564–0.687) and 0.683 (0.622–0.740), respectively, and in HBeAg-negative patients were 0.681 (0.618–0.740) and 0.702 (0.639–0.760), and 0.569 (0.503–0.633) and 0.630 (0.565–0.691), respectively. Conclusion. Following hepatic aggravation of necroinflammation and progression of fibrosis, anti-HBc increases gradually in HBeAg-positive patients and continues to increase gradually in HBeAg-negative patients, which is a useful but unsatisfactory marker for monitoring pathological states.


2010 ◽  
Vol 17 (6) ◽  
pp. 1048-1053 ◽  
Author(s):  
Yi-Hsiang Huang ◽  
Hung-Hsu Hung ◽  
Che-Chang Chan ◽  
Chiung-Ru Lai ◽  
Chi-Jen Chu ◽  
...  

ABSTRACT Intrahepatic hepatitis B virus (HBV) core antigen (HBcAg) is a hallmark of viral replication in hepatitis B virus e antigen (HBeAg)-positive chronic hepatitis B (CHB). The aim of this study was to evaluate the role of HBcAg in HBeAg-negative CHB. One hundred six HBeAg-negative CHB patients who underwent ultrasonographically guided liver biopsy were reviewed for their HBV DNA load and clinical and histological data. Factors associated with the expression of intrahepatic HBcAg were analyzed. Among the patients, 35 (33%) were positive for HBcAg by immunohistostaining. In patients whose HBV DNA loads were higher than 107 copies (cp)/ml, nearly one-half (52%) had detectable HBcAg. Compared with HBcAg-negative patients, HBcAg-positive patients had higher serum alanine transaminase (ALT) and HBV DNA levels and more-severe hepatic necroinflammation. High serum ALT level (>160 U/liter) and HBV viral load were the determinants of HBcAg expression in multivariate analysis. Large amounts of HBcAg expression were frequently detected in patients with high DNA loads, and the patterns of HBcAg distribution were not related to histological activity or HBV DNA levels. In patients with lower HBV DNA loads, the expression of HBcAg was the key factor associated with active hepatic necroinflammation (hazard ratio = 11.25; 95% confidence interval [CI], 1.42 to 89.26; P = 0.022). In conclusion, the expression of HBcAg is not frequent in HBeAg-negative CHB. The expression of intrahepatic HBcAg indicates active hepatic necroinflammation, even in patients with low HBV DNA load. Both HBV viral load and HBcAg expression have implications in the pathogenesis of HBeAg-negative CHB.


2008 ◽  
Vol 6 (5) ◽  
pp. 275-280 ◽  
Author(s):  
Nicolaos C. Tassopoulos ◽  
Maria H. Sjogren ◽  
John R. Ticehurst ◽  
Ronald E. Engle ◽  
Anastasia Roumeliotou-Karayannis ◽  
...  

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