Hepatitis B e Antigen Seroconversion: A Critical Event in Chronic Hepatitis B Virus Infection

Abstract

It was agreed that HBeAg seroconversion is an important serologic end point for patients with CHB and that achieving this goal should be an important consideration in treatment selection. Patients with HBeAg-positive CHB should consider pegylated interferon if they are aged < 40 years (especially women), have lower HBV DNA levels, can afford this treatment, and have a lifestyle that would support adherence to injection therapy. Alternatively, nucleos(t)ide analogs are recommended in patients with alanine aminotransferase levels ≥ 2 × the upper limit of normal, HBV DNA levels < 9 log(10) IU/ml, and compensated CHB. Entecavir, telbivudine, and tenofovir may be used as first-line therapy; they can be administered as a finite therapeutic course in HBeAg-positive patients who seroconvert. Telbivudine and tenofovir should be considered in women of child-bearing potential.

Chronic Hepatitis B Virus Infection in Children and Adolescents in Japan

“…Asians, mother-to-child transmission, and genotype C are considered to be unfavorable factors for HBeAg seroconversion (19,20). All of the children in our study were Asian.…”

Development of immunity against hepatitis B virus after donor lymphocyte infusion in a peripheral blood stem cell transplantation recipient with chronic hepatitis B

“…Anti-viral therapy alone was ineffective in clearing her HBV. This is not unexpected, since the 2-year cumulative HBeAg seroconversion rate was around 30% on oral nucleos(t)ide analog [13] and antiviral therapy alone seldom leads to HBsAg clearance in Asian patients [14]. Concurrent antiviral drugs additional to adoptive immunity transfer by BMT would be beneficial for clearing HBV [15,16].…”

Hepatitis B virus basal core promoter mutations show lower replication fitness associated with cccDNA acetylation status

“…The in vivo studies utilised HBeAg as a marker of viral replication. However, during HBeAg seroconversion, viral loads fluctuate significantly due to complex viral immune responses and therefore HBeAg levels cannot represent viral replication (Chu and Liaw, 2007;Liaw et al, 2010). Furthermore, cell based studies have employed plasmids containing either subgenomic mutated fragments isolated from different genetic backgrounds or infectious clones with the mutations generated by site-directed mutagenesis.…”