Abstract
Hepatitis B virus (HBV) contains three viral surface proteins, large, middle and small hepatitis B surface protein (LHBs, MHBs, SHBs). Proportions of LHBs and MHBs are lower in patients with inactive vs active chronic infection. Interferon alfa may convert hepatitis B e antigen (HBeAg)-positive chronic hepatitis B (CHB) to an inactive carrier state, but prediction of sustained response is unsatisfactory. The aim of this study was to test the hypothesis that quantification of MHBs and LHBs may allow for a better prognosis of therapeutic response than total hepatitis B surface antigen (HBsAg) concentration. Hepatitis B surface proteins were measured before and during peginterferon alfa-2a therapy in serum from 127 Asian patients with HBeAg-positive CHB. Sustained response was defined as HBeAg seroconversion 24weeks post-treatment. Mean total HBs levels were significantly lower in responders vs nonresponders at all time points (P<.05) and decreased steadily during the initial 24weeks treatment (by 1.16 vs 0.86ng/mL in responders/nonresponders respectively) with unchanged relative proportions. Genotype B had a two-fold higher proportion of LHBs than genotype C (13% vs 6%). HBV DNA, HBeAg, HBsAg and HBs protein levels predicted response equally well but not optimally (area under the receiver operating characteristic curve values >0.70). Hepatitis B surface protein levels differ by HBV genotype. However, quantification of HBs proteins has no advantage over the already established HBsAg assays to predict response to peginterferon alfa-2a therapy in HBeAg-positive patients.
Highlights
Hepatitis B virus (HBV) surface antigen (HBsAg) is essential for diagnosis of HBV infection
We have examined the variation in levels of different hepatitis B surface antigen (HBsAg) components in patients with hepatitis B e antigen (HBeAg)-positive chronic hepatitis B (CHB) treated with peginterferon alfa-2a, according to treatment response
This study provides insight into the proportions of hepatitis B surface (HBs) proteins in the serum of patients with HBeAg-positive CHB, their kinetics during pegylated interferon alfa (PegIFN) treatment, and their utility in predicting treatment response
Summary
Hepatitis B virus (HBV) surface antigen (HBsAg) is essential for diagnosis of HBV infection. HBsAg consists of three co-carboxyterminal proteins: large (L), middle (M), and small (S) HBs proteins (Supplementary Figure 1A). SHBs is the major component of the virion envelope and SVPs.[5] The exterior hydrophilic loop of the multiple membrane-spanning S domain forms the major antigenic determinants of HBsAg. MHBs is nonessential for replication,[7] but is conserved in all known orthohepadnaviruses, the genus of HBV.[5] MHBs has been detected in HBeAg-positive chronic HBV carriers but was not as readily detectable in HBeAg-negative carriers,[9,10] suggesting a correlation and a potential synergism between MHBs and HBeAg expression. Pfefferkorn et al.[11] recently reported that HBsAg carriers with long-term stable inactive HBV infection have significantly lower LHBs and MHBs levels compared with chronic hepatitis B patients, irrespective of HBeAg status. The aim of this study was to test the hypothesis that quantification of MHBs and LHBs may allow for a better prognosis of therapeutic response than total hepatitis B surface antigen (HBsAg) concentration
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