Seroconversion from hepatitis B e antigen to anti-HBe in chronic hepatitis B virus infection

Realdi, Giuseppe; Alberti, Alfredo; Rugge, Massimo; Bortolotti, Flavia; Rigoli, A; Tremolada, F.; Ruol, A

doi:10.1016/0016-5085(80)90130-4

Cited by 406 publications

(126 citation statements)

References 13 publications

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“…Studies conducted in tertiary care centres in Europe among patients with compensated cirrhosis showed that those with persistently high levels of HBV replication, as indicated by HBeAg positivity, have increased liver related death rates, of about 2-fold, as compared to those who clear HBeAg with biochemical remission 5. Early studies on the natural history of chronic hepatitis B in Caucasian patients do not provide information whether HBeAg seroconversion leads to a decreased risk of liver-related adverse events and mortality, due to the too short follow-up period of 5 years at most8 17 18…”

Section: Discussionmentioning

confidence: 99%

Long-term outcome of chronic hepatitis B in Caucasian patients: mortality after 25 years

Fattovich

Olivari

Pasino

et al. 2007

Gut

216

203

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Section: Discussionmentioning

confidence: 99%

Long-term outcome of chronic hepatitis B in Caucasian patients: mortality after 25 years

Fattovich

Olivari

Pasino

et al. 2007

Gut

216

203

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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].…”

Section: Natural History Of Chronic Hbv Infectionmentioning

confidence: 99%

Mechanisms of HBV-related hepatocarcinogenesis

Neuveut

Buendia

2010

Journal of Hepatology

376

308

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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.

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“…23 However, reactivation of HBV occasionally occurs in such HBsAg-positive and anti-HBe-positive individuals under certain immunosuppressive conditions, sometimes resulting in lethal hepatic failure. [9][10][11][12][13] Several recent studies have, however, demonstrated the reactivation of HBV in HBsAg-negative and anti-HBcpositive healthy individuals.…”

Section: Discussionmentioning

confidence: 99%

Reactivation of latently infected hepatitis B virus in a leukemia patient with antibodies to hepatitis B core antigen

Marusawa

Imoto

Ueda

et al. 2001

Journal of Gastroenterology

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A 66-year-old man with chronic B-cell leukemia who had antibody to hepatitis B core antigen (anti-HBc) but not hepatitis B surface antigen (HBsAg) suffered from lethal hepatitis caused by hepatitis B virus (HBV) reactivation. He initially lacked circulating viral genomes in his sera and did not have a past history of liver dysfunction. In this patient, the immunosuppressive condition introduced by disease progression of leukemia induced reactivation of dormant HBV, and the withdrawal of chemotherapy resulted in fatal liver failure. Mutation-specific assay based on competitive polymerase chain reaction (PCR) and sequencing analyses revealed the predominant reactivation of an HBV strain with missence mutation (point mutation G-to-A at nucleotide 1896) in the precore regions, as well as point mutations in the core promoter regions. Therefore, it is important to note the risk of HBV reactivation, with resulting lethal hepatic failure, in anti-HBc-positive healthy individuals, even when they lack HBsAg. who receive immunomodulating therapy.

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Seroconversion from hepatitis B e antigen to anti-HBe in chronic hepatitis B virus infection

Cited by 406 publications

References 13 publications

Long-term outcome of chronic hepatitis B in Caucasian patients: mortality after 25 years

Long-term outcome of chronic hepatitis B in Caucasian patients: mortality after 25 years

Mechanisms of HBV-related hepatocarcinogenesis

Reactivation of latently infected hepatitis B virus in a leukemia patient with antibodies to hepatitis B core antigen

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