Chronic hepatitis B surface antigen seroclearance‐related immune factors

Abstract

The ultimate aims of the treatment of hepatitis B virus infection are the loss of hepatitis B surface antigen (HBsAg) and hepatitis B surface antibody seroconversion. Unfortunately, these goals are rarely reached. Many factors are associated with HBsAg seroconversion, including genetic, immune, and viral factors. However, the mechanism of HBsAg seroclearance, and particularly the immune mechanism, is still difficult to elucidate. The immune factor interferon-α is currently the main antiviral therapy for chronic hepatitis B virus infection. However, a sustained shift from response of HBsAg to hepatitis B surface antibody seroconversion is rarely obtained. Recent studies have revealed that several of the newly identified immune factors are closely related to the removal of HBsAg. In this article, we review recent studies on these immune factors, their influence on hepatitis B progression, and HBsAg seroconversion.

Precore G1896A mutation is associated with reduced rates of HBsAg seroclearance in treated HIV hepatitis B virus co‐infected patients from Western Africa

“…HBsAg seroclearance is mainly viewed as the consequence of complex and appropriate immune responses during the course of infection. 31 NA-based therapy does not have substantial immunomodulatory effects compared to other treatment options, such as pegylated interferon. 32 Regardless, higher rates of HBsAg seroclearance are often observed during HBeAg-positive phases of HBV when patients are undergoing treatment with any antiviral agent.…”

“…We defined the "baseline" visit at ART-initiation and "follow-up" visits at each yearly visit thereafter until the date A1762T/G1764A mutations (P < .001). Patients were followed for a median 36 months (IQR = [24][25][26][27][28][29][30][31][32][33][34][35][36]. Cumulative proportion of undetectable HBV-DNA was significantly higher in patients with baseline mutation (pcG1896A = 86.6% vs no pcG1896A = 66.9%, P = .04), but not after adjusting for baseline HBV-DNA levels and anti-HBV agent (P = .2).…”

Stopping long‐term treatment with nucleos(t)ide analogues is a favourable option for selected patients with HBeAg‐negative chronic hepatitis B

“…The exact mechanism of HBsAg seroclearance is still unclear, and there is no targeted treatment to achieve this endpoint . However, the evaluation of NA treatment withdrawal in patients with HBeAg‐negative hepatitis B studies has shown higher HBsAg loss rates than in studies with long‐term NA or combined NA and pegylated interferon alfa.…”

Analysis of hepatitis B surface antigen (HBsAg) using high‐sensitivity HBsAg assays in hepatitis B virus carriers in whom HBsAg seroclearance was confirmed by conventional assays

“…The function of regulatory T cells is reduced in patients given NA therapy owing to a decrease in the helper T cell‐mediated ability of B cells to produce antibodies. In untreated patients, HBV is reduced by elimination of HBV‐infected liver cells through natural immunity . In contrast, the main anti‐HBV activity of NA is inhibition of reverse transcriptase .…”

“…In untreated patients, HBV is reduced by elimination of HBV-infected liver cells through natural immunity. [41][42][43] In contrast, the main anti-HBV activity of NA is inhibition of reverse transcriptase. 44 Therefore, there may be differences in the amounts of cccDNA at the time of HBsAg seroclearance between cases of natural elimination and cases of elimination by NA therapy, and release of trace amounts of HBsAg may be more likely to occur from the remaining cccDNA.…”