Seroconversion from HBe antigen to anti-HBe in chronic HBV infection

Gastroenterology (Impact Factor: 16.72). 09/1980; 79(2):195-9.
Source: PubMed


Among 116 patients with chronic hepatitis B virus infection and biopsy-proved chronic liver disease, the prevalence of hepatitis B e antigen (HB(e)Ag) in serum was higher in the cases with chronic active hepatitis without cirrhosis compared with those with chronic active hepatitis who had already progressed to cirrhosis. Accordingly, the opposite trend was noted in the prevalence of antibody to the hepatitis B e antigen (anti-HB(e)). The mean age of the HB(e)Ag-positive patients was significantly lower than that of the cases with anti-HB(e); in addition, the duration of the illness at the time of testing was apparently longer in the latter group, as assessed by the prevalence of an acute onset in the recent history. Fifty of the 116 patients were followed longitudinally over a period ranging from 2 to 7 yr; of the 29 cases initially HB(e)Ag-positive, 13 eventually lost the antigen, and 10 of them seroconverted to anti-HB(e). Seroconversion was always associated with a striking reduction in the activity of virus replication and prevailed in patients who progressed to cirrhosis. Transaminase levels improved in all the cases who seroconverted, independently of the histological evolution. These results suggest that in HB(s)Ag-positive chronic active hepatitis presence of HB(e)Ag in serum identifies an early, although prolonged, phase of active virus replication that is frequently followed by the disappearance of complete virus particles from serum and appearance of anti-HB(e). In these patients this event does not imply a good prognosis as it occurred mainly in those who developed cirrhosis. Immunosuppressive treatment appeared, in our experience, to delay seroconversion, but not to affect its incidence.

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    • "Senescence in tumourigenesis is regarded as a defense mechanism and evasion of senescence is thought to lead to malignancy [38]. Among patients in the ''immune active phase " , a majority eventually progress into the ''inactive HBV carrier phase " , characterized by loss of HBeAg, seroconversion to anti-HBe antibodies and decline of serum HBV DNA to barely detectable levels, as well as improvement of fibrosis and inflammation over time [35] [39] [40]. In prospective studies, this state has been associated with a favorable long-term outcome [41]. "
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    ABSTRACT: The hepatitis B virus (HBV) is a small enveloped DNA virus, which primarily infects hepatocytes and causes acute and persistent liver disease. Epidemiological studies have provided overwhelming evidence for a causal role of chronic HBV infection in the development of hepatocellular carcinoma, but the molecular mechanisms underlying virally-induced tumourigenesis remain largely debated. In the absence of a dominant oncogene encoded by the HBV genome, indirect roles have been proposed, including insertional activation of cellular cancer-related genes by HBV DNA integration, induction of genetic instability by viral integration or by the regulatory protein HBx, and long-term effects of viral proteins in enhancing immune-mediated liver disease. Recent genetic studies indicate that HBV-related tumours display a distinctive profile with a high rate of chromosomal alterations and low frequency of beta-catenin mutations. This review will discuss the evidence implicating chronic HBV infection as a causal risk factor of primary liver cancer. It will also discuss the molecular mechanisms that are critical for the tumourigenic process due to long lasting infection with HBV.
    Journal of Hepatology 04/2010; 52(4):594-604. DOI:10.1016/j.jhep.2009.10.033 · 11.34 Impact Factor
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    • "With a population of 150 million, Bangladesh has a high HBsAg positivity in adults (7.3–7.5%).[89] HBeAg-negative is an important form of chronic hepatitis B (CHB).[1011] This form of CHB is being increasingly reported worldwide.[12–19] "
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    Saudi Journal of Gastroenterology 01/2008; 14(1). DOI:10.4103/1319-3767.37796 · 1.12 Impact Factor
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    ABSTRACT: Seventy consecutive HBsAg- and HBeAg-positive patients with biopsy-proven chronic hepatitis were followed prospectively with serial determinations of SGPT levels and hepatitis B virus serum markers including HBsAg, HBeAg, anti-HBe and hepatitis B virus DNA. During a period of 1 to 11 years (mean +/- S.D.: 5.0 +/- 2.3 years), 28 patients remained persistently HBeAg positive, most with continuing biochemical and histologic activity, while 41 cases seroconverted to anti-HBe. One patient became HBeAg and anti-HBe negative. After seroconversion, 87.8% of the cases showed sustained normalization of SGPT, and clearance of hepatitis B virus DNA from serum and histologic improvement was documented in 79% of the cases who had a control liver biopsy, while 15.8% developed cirrhosis. In two patients (4.9%), the disease remained active despite seroconversion, and both cases had evidence of continuing hepatitis B virus replication. Finally, reactivation of liver damage and of hepatitis B virus replication was observed in three additional patients (7.3%) who had transiently normalized SGPT after seroconversion. All 70 patients were analyzed for hepatitis delta virus markers, and only two persistently HBeAg-positive cases were found positive for antibody to hepatitis delta virus in serum, one also having hepatitis delta antigen in the liver. These findings indicate that, in chronic hepatitis type B, termination of virus replication is associated in most patients with biochemical and histologic regression of inflammatory activity. After anti-HBe seroconversion has occurred, virus replication and liver disease may persist or reactivate in a small proportion of patients thus giving origin to the well-recognized group of anti-HBe positive, hepatitis B virus DNA-positive chronic hepatitis type B.
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