Correlation between Hepatitis B surface antigen titers and HBV DNA levels

Alghamdi, Abdulaziz G.; Aref, Nagwa; El‐Hazmi, Mohsen A. F.; Al–Hamoudi, Waleed; Alswat, Khalid; Helmy, Ahmed; Sanai, Faisal M.; Abdo, Ayman A.

doi:10.4103/1319-3767.121035

Cited by 32 publications

(26 citation statements)

References 29 publications

(32 reference statements)

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“…[ 15 – 17 ] However, HBeAg is still qualitatively assayed despite advances in quantitative detection of HBsAg. [ 18 ] Furthermore, a truly quantitative relationship between HBeAg and HBV DNA levels remains to be established. In this study, we conducted a large-scale community-based screening of HBV-infected individuals by random collection of blood samples from the entire populations of 12 villages.…”

Section: Introductionmentioning

confidence: 99%

Serum HBeAg and HBV DNA levels are not always proportional and only high levels of HBeAg most likely correlate with high levels of HBV DNA

et al. 2017

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This study aimed to investigate the correlation between quantitative hepatitis B e antigen (HBeAg) and hepatitis B virus (HBV) DNA levels, and to determine whether semiquantitative measurement of HBeAg can indicate the extent of HBV replication in HBeAg-positive subjects in the immune tolerant phase.A cross-sectional, community-based survey was carried out in 12 communities of 2 counties in Zhejiang Province, China. A panel of 788 HBeAg-positive subjects was divided into 4 groups according to HBV DNA level.Groups I (n = 111), II (n = 91), III (n = 124), and IV (n = 462) had HBV DNA levels below 103 copies/mL (PCR undetectable), between 103 and 105 copies/mL (PCR detectable), between 105 and 2 × 107 copies/mL (hybridization detectable), and >2 × 107 copies/mL, respectively. The HBeAg level correlated well with the HBV DNA level (R2 = 0.658; P < .01) on a log scale. The average HBeAg level in group IV was significantly higher than those in the other 3 groups, and the best HBeAg cut-off value for differentiating group IV from the other 3 groups was 768 S/CO, with a sensitivity of 94.4% and specificity of 91.1%.Semiquantification of HBeAg could indicate a relative HBV DNA level in HBeAg-positive subjects in the immune tolerant phase.

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Section: Introductionmentioning

confidence: 99%

Serum HBeAg and HBV DNA levels are not always proportional and only high levels of HBeAg most likely correlate with high levels of HBV DNA

et al. 2017

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“…The level of HBeAg was evaluated using the S/CO, and HBeAg positivity was confirmed in those with an S/CO ≥1.0. [ 36 ] A sub-analysis showed that patients who received consolidation therapy for 18 months and had a baseline level of HBeAg >1000 S/CO experienced a significantly lower risk of relapse. In other words, a prolonged consolidation period was beneficial to patients with a high baseline semi-quantitative level of HBeAg in terms of off-treatment durability.…”

Section: Discussionmentioning

confidence: 99%

Consolidation period of 18 months no better at promoting off-treatment durability in HBeAg-positive chronic hepatitis B patients with tenofovir disoproxil fumarate treatment than a 12-month period

et al. 2020

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There has been no clear consensus on the optimal consolidation periods following HBeAg seroconversion (SC) in HBeAg-positive chronic hepatitis B (CHB) patients. Our study aimed to prospectively compare relapse rates between 12 months’ and 18 months’ consolidation periods to see whether or not there is beneficial durability of tenofovir disoproxil fumarate (TDF) therapy with longer consolidation periods. We enrolled a total of 137 HBeAg-positive Asian CHB patients treated with TDF monotherapy. Forty-six patients achieved HBeAg SC. Then, they were randomly assigned to consolidation period of either 12 months (group A) or 18 months (group B). After stopping TDF therapy, all patients were followed up for 12 months. Thirteen patients (56.5%) relapsed in group A and 12 patients (52.2%) relapsed in group B after 12 months’ follow-up ( P = .958). Pretreatment HBsAg level is the only significant predictor for off-therapy recurrence by univariate analysis ( P = .024). Baseline HBeAg >1000 S/CO in group B patients were significantly less likely to relapse than those of group A ( P = .046). Baseline alanine aminotransferase (ALT) >133 U/L could significantly predict occurrence of HBeAg SC ( P = .008; 95% CI: 0.545–0.763; AUC: 0.654). Overall, a prolonged consolidation period has no positive effect on TDF therapy on sustained viral suppression in HBeAg-positive Asian CHB patients. However, a prolonged consolidation period was beneficial to patients with high baseline semi-quantitative HBeAg levels in terms of off-treatment durability. Baseline ALT > 133 U/L could significantly predict the occurrence of HBeAg SC.

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“…Relative to other parts of the world, the prevalence of HBV in Iran varies from low to intermediate based on geographic region. Although there are an estimated 1.5 million chronically infected individuals ( 5 ), the rate of liver cancer is lower than might be expected, perhaps explained by a higher prevalence of genotype D, and high prevalence of HBeAg seronegativity or because of some mutations in core or pre-core region of the virus ( 10 , 11 ). On the other hand, HBV positive individuals in Middle Eastern countries have been shown to have a high susceptibility for acquisition of pre-core or basal core promoter variants that may affect HBeAg ( 10 ), but perhaps not HBV replication or other aspects of HBV.…”

Section: Introductionmentioning

confidence: 99%

Association of Mutations in the Basal Core Promoter and Pre-core Regions of the Hepatitis B Viral Genome and Longitudinal Changes in HBV Level in HBeAg Negative Individuals: Results From a Cohort Study in Northern Iran

et al. 2015

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Background:Although certain HBV mutations are known to affect the expression of Hepatitis e antigen, their association with HBV viral level or clinical outcomes is less clear.Objectives:We evaluated associations between different mutations in the Basal Core promoter (BCP) and Pre-core (PC) regions of HBV genome and subsequent changes in HBV viral DNA level over seven years in a population of untreated HBeAg negative chronic hepatitis B (CHB) participants in Northeast of Iran.Materials and Methods:Participants in the current study were drawn from the Golestan Hepatitis B Cohort Study (GHBCS), a cohort of approximately 2590 HBsAg positive subjects (living in Gonbad city) embedded in the Golestan Cohort Study (GCS). At baseline, HBsAg was measured in all participants and revealed 2590 HBsAg positive cases. We randomly selected 304 participants who their blood sample were taken at both baseline and seven years later in follow-up and had not been treated for HBV during this time. HBV viral load were assessed at baseline and at year 7. The BCP and PC regions of the HBV DNA, at baseline, were amplified via hemi-nested PCR and sequenced by cycle sequencing. At year 7, liver stiffness was assessed by fibroscan; also, other parameters of liver disease were assessed following standard clinical protocols. Associations were assessed via tabulation, chi-square, t-tests and logistic regression. P values < 0.05 were considered statistically significant and all tests were two-sided.Results:Among 304 HBsAg positive participants, 99 had detectable HBV DNA at study baseline. Of these, 61.6% had PC mutations (48.5% A1896 and 25.2% G1899). In contrast to other mutations, A1896 was associated with a higher proportion of detectable HBV DNA at year 7 (39.6%) compared to patients with the wild type (13.7%) (OR: 4.36, CI95% = 1.63-11.70; P Value = 0.002). Although participants with the A1896 mutation had higher year-7 HBV viral load than participants with G1896 (2.30 ± 1.66 IU/mL vs. 1.76 ± 1 IU/mL among patients with detectable HBV; P value = 0.052), no association was observed with either serum level ALT or liver stiffness. Interestingly, mutations in the basal core promoter (BCP) region had no significant effect on virus DNA detection.Conclusions:In this population with chronic HBeAg negative hepatitis B, an association was observed between the G1896A mutation in the Pre-core region of HBV and subsequent level of HBV DNA seven years later, which indicated that mutations in this region of HBV genome may contribute to disease progression in these patients and play an important role in HBV natural course of disease.

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Correlation between Hepatitis B surface antigen titers and HBV DNA levels

Cited by 32 publications

References 29 publications

Serum HBeAg and HBV DNA levels are not always proportional and only high levels of HBeAg most likely correlate with high levels of HBV DNA

Serum HBeAg and HBV DNA levels are not always proportional and only high levels of HBeAg most likely correlate with high levels of HBV DNA

Consolidation period of 18 months no better at promoting off-treatment durability in HBeAg-positive chronic hepatitis B patients with tenofovir disoproxil fumarate treatment than a 12-month period

Association of Mutations in the Basal Core Promoter and Pre-core Regions of the Hepatitis B Viral Genome and Longitudinal Changes in HBV Level in HBeAg Negative Individuals: Results From a Cohort Study in Northern Iran

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