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[Can HBsAg levels guide to differentiate inactive HBsAg carriers from HBeAg negative chronic B hepatitis?]
Murat Sayan1, Birsen Mutlu, Sarper Erdoğan
1Kocaeli Universitesi Tip Fakültesi, Merkez Laboratuvan PCR Unitesi, Kocaeli. sayanmurat@hotmail.com
Insights
Hepatitis B virus (HBV) S/N levels can help distinguish inactive HBsAg carriers from chronic hepatitis B (CHB) cases with high viral loads. Further research with quantitative HBsAg measurements is needed to confirm this finding.
Area of Science:
- Hepatology
- Virology
- Immunology
Context:
- Differentiating inactive Hepatitis B surface antigen (HBsAg) carriers from HBeAg-negative chronic hepatitis B (CHB) is clinically important.
- CHB can arise from precore or core promoter mutations in the Hepatitis B virus (HBV).
Purpose:
- To investigate the utility of HBsAg S/N levels in differentiating inactive HBsAg carriers from HBeAg-negative CHB cases.
Summary:
- A study of 134 HBsAg-positive patients classified them into four groups based on serological markers and ALT levels.
- Mean HBsAg S/N levels were significantly higher in HBeAg-negative CHB patients with HBV-DNA >10^5 copies/mL compared to inactive carriers.
- No significant difference in HBsAg S/N levels was observed between inactive carriers and HBeAg-negative CHB patients with lower HBV-DNA levels.
Impact:
- HBsAg S/N levels may aid in distinguishing inactive HBsAg carriers from CHB patients with high viral loads.
- Further studies using quantitative HBsAg measurements (IU/mL) and mutation analysis in larger cohorts are warranted.
Abstract:
It is valuable to differentiate the inactive HBsAg carrier state from HBeAg negative chronic B hepatitis (CBH) which develops due to precore or core promoter region mutations in hepatitis B virus (HBV). The aim of this study was to investigate the role of HBsAg S/N (sample rate/index calibrator mean rate) levels in the differentiation of inactive HBsAg carriers from HBeAg negative CBH cases. A total of 134 HBsAg positive patients followed-up in Kocaeli University Medical Faculty hospital between June 2004-September 2005, were included to the study. The patients were classified into four groups according to their serological patterns (Group 1: HBeAg and HBV-DNA negative 34 cases with normal ALT levels; Group 2: HBeAg negative, anti-HBe positive, HBV-DNA >10(5) copies/ml, 36 cases with increased ALT levels; Group 3: HBeAg negative, anti-HBe positive, HBV-DNA 102-10(5) copies/ml, 32 cases with normal ALT levels; Group 4: HBeAg positive, HBV-DNA >10(5) copies/ml, 32 cases with increased ALT levels). The age and gender distributions of the groups were similar. HBV markers have been detected by microparticle enzyme immunoassay (AxSYM System, v3.0, Abbott Laboratories, USA), and viral load were investigated by real-time polymerase chain reaction (iCycler IQ, v3.0a, Bio Rad Laboratories, USA). As a result, the mean HBsAg S/N level in group 2 who were HBeAg negative with a viral load of >10(5) copies/ml, was found significantly higher than group 1 who were inactive HBsAg carriers (285.9+/-78.8 and 214.4+/-108.6, respectively; p<0.05). In contrast there was no statistically significant difference between group 1 (HBV-DNA negative) and group 3 (HBV-DNA <10(5) copies/mL) by means of mean HBsAg S/N levels (214.4+/-108.6 and 216.3+/-57.2, respectively; p>0.05). Although HBsAg levels seem to guide the differentiation of inactive HBsAg carriers from HBeAg negative CBH cases with high viral loads (>10(5) copies/ml), advanced studies are needed to clarify this relationship with the use of quantitative HBsAg measurements (IU/ml) in large patient groups and by performing mutation analysis.
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