Dane particle DNA polymerase and HBeAg: Impact on clinical, laboratory, and histologic findings in hepatitis B-associated chronic liver disease

Andres, Ljudevit L.; Sawhney, Vinod K.; Scullard, George; Smith, Joseph L.; Merigan, Thomas C.; Robinson, William S.; Gregory, Peter B.

doi:10.1002/hep.1840010604

Cited by 17 publications

(5 citation statements)

References 19 publications

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“…17 HBV genomic DNA in the sera of infected mice also exhibited a dose-dependent correlation. The HBV DNA levels, ranging from 6.61×10 6 to 7.20×10 7 copies/ml in the mice infected with 1×10 11 vg AAV/HBV (Figure 1e), are comparable to those of CHB patients in the immunotolerant stage.…”

Section: Resultsmentioning

confidence: 84%

A mouse model for HBV immunotolerance and immunotherapy

et al. 2013

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Lack of an appropriate small animal model remains a major hurdle for studying the immunotolerance and immunopathogenesis induced by hepatitis B virus (HBV) infection. In this study, we report a mouse model with sustained HBV viremia after infection with a recombinant adeno-associated virus (AAV) carrying a replicable HBV genome (AAV/HBV). Similar to the clinical HBV carriers, the mice infected with AAV/HBV were sero-negative for antibodies against HBV surface antigen (HBsAg). Immunization with the conventional HBV vaccine in the presence of aluminum adjuvant failed to elicit an immune response against HBV in these mice. To identify a vaccine that can potentially circumvent this tolerance, the TLR9 agonist CpG was added to HBsAg as an adjuvant. Vaccination of mice with HBsAg/CpG induced not only clearance of viremia, but also strong antibody production and T-cell responses. Furthermore, both the DNA replication and protein expression of HBV were significantly reduced in the livers of AAV/HBV-infected mice. Accordingly, AAV/HBV-infected mice may be used as a robust model for investigating the underlying mechanism(s) of HBV immunotolerance and for developing novel immunotherapies to eradicate HBV infections.

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Section: Resultsmentioning

confidence: 84%

A mouse model for HBV immunotolerance and immunotherapy

et al. 2013

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“…HBeAg was observed to be present during the initial phase of chronic HBV infection, and its presence correlated with the detection of HBV DNA polymerase activity and HBV DNA in serum 6, 7. In some patients, spontaneous HBeAg to HBe antibody (anti‐HBe) seroconversion occurred during the course of chronic HBV infection 8, 9.…”

Section: Natural History Of Chronic Hepatitis B Virus Infection: Whatmentioning

confidence: 95%

Natural History of Chronic Hepatitis B Virus Infection: What We Knew in 1981 and What We Know in 2005

2006

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Natural History of Chronic Hepatitis B Virus Infection: What We Knew in 1981Progression From Acute to Chronic Infection. Epidemiological and clinical studies estimated that approximately 10% of patients with acute hepatitis B virus (HBV) infection progress to chronic infection. 1 Recovery from acute HBV infection with hepatitis B surface antigen (HBsAg) to antibody (anti-HBs) seroconversion was thought to indicate virus clearance.Markers of HBV Replication and Significance of Hepatitis B e Antigen. In 1981, evaluation of hepatitis B patients relied on serology assays. 2,3 It was recognized that infectivity of HBV carriers varied and hepatitis B e antigen (HBeAg) was a reliable marker of infectivity. 3 HBV was known to be a DNA virus, and many investigators were developing assays to measure HBV DNA polymerase activity and later HBV DNA level. [4][5][6] These assays relied on hybridization techniques with a lower limit of detection of approximately 10 6 copies/mL, and most assays were semi-quantitative. 5,6

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“…A serologic evolution of HBV infection has been proposed in which the presence of HBeAg indicates an early and prolonged phase of active viral replication with high hepatitis B surface antigen (HBsAg) and HBV DNA levels 7–9. With time, many patients spontaneously convert to low viral replication, an event associated with a decrease in HBV DNA levels, loss of HBeAg, development of antibody to hepatitis B e antigen (anti‐HBe), and decreased aminotransferase levels 10, 11.…”

mentioning

confidence: 99%

Histopathology and clinical correlates of end-stage hepatitis B cirrhosis: A possible mechanism to explain the response to antiviral therapy

Sigal

Ala²,

Ivanov³

et al. 2004

Liver Transpl

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In chronic liver disease associated with histological necroinflammation, clinical severity is frequently greater in those with higher grades of activity. Conventional wisdom assumes that necroinflammation is mild or absent in patients with end-stage hepatitis B virus (HBV) cirrhosis due to the frequent presence of mildly elevated aminotransferase levels, the absence of hepatitis B e antigen (HBeAg), and low or undetectable HBV deoxyribonucleic acid (DNA) levels. However, a histopathologic analysis of such patients has not been undertaken. The aims of this study were 1) to assess severity and histological features of inflammation, 2) to correlate the severity of inflammation with biochemical and virologic parameters, and 3) to define the relationship between inflammation and clinical severity in explanted livers from patients undergoing liver transplantation for HBV cirrhosis. Characteristics of 34 consecutive patients undergoing liver transplantation for HBV cirrhosis were correlated with inflammation and immunohistological findings in the explanted livers. High-grade inflammation (grades 3 and 4) was found in many cases (47.1% interface hepatitis; 14.8% lobular inflammation; and 20.6% portal inflammation). The presence of positive cytoplasmic staining for hepatitis B core antigen (HBcAg) was associated with grade 3 or 4 interface hepatitis (P ‫؍‬ .046) and lobular hepatitis (P ‫؍‬ .005). There was no correlation between inflammatory activity and age, Asian ethnicity, aminotransferase levels, total bilirubin levels, HBeAg seropositivity, and detect-

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Dane particle DNA polymerase and HBeAg: Impact on clinical, laboratory, and histologic findings in hepatitis B-associated chronic liver disease

Cited by 17 publications

References 19 publications

A mouse model for HBV immunotolerance and immunotherapy

A mouse model for HBV immunotolerance and immunotherapy

Natural History of Chronic Hepatitis B Virus Infection: What We Knew in 1981 and What We Know in 2005

Histopathology and clinical correlates of end-stage hepatitis B cirrhosis: A possible mechanism to explain the response to antiviral therapy

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