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. 2025 Jul 30;232(1):e64-e72.
doi: 10.1093/infdis/jiaf190.

Circulating Hepatitis B Virus (HBV) RNA and Conventional Markers in Treatment-Naive Persons With HBV in Senegal

Collaborators, Affiliations

Circulating Hepatitis B Virus (HBV) RNA and Conventional Markers in Treatment-Naive Persons With HBV in Senegal

Lorin Begré et al. J Infect Dis. .

Abstract

Background: Hepatitis B virus (HBV) infection affects approximately 10% of the general population in West Africa. Circulating HBV RNA may help improve the characterization of HBV disease and prognosis. We aimed to evaluate the associations between HBV RNA and conventional biomarkers of HBV replication in the Senegalese Hepatitis B Cohort Study (SEN-B).

Methods: We included all treatment-naive, human immunodeficiency virus-negative participants of SEN-B with chronic HBV infection confirmed by a quantitative hepatitis B surface antigen (HBsAg) >0.05 IU/mL. We quantified HBV RNA, HBV DNA, and HBsAg levels and evaluated associations between those markers stratified by HBV infection phase, alanine aminotransferase level, and liver fibrosis stage.

Results: Of 719 participants, 17 (2.4%) were hepatitis B e antigen (HBeAg)-positive (EP), 620 (86.2%) were classified as HBeAg-negative chronic infection (ENCI), and 82 (11.4%) were classified as HBeAg-negative chronic hepatitis (ENCH). HBV RNA was undetectable in 361 (49.8%) participants, and detectable but unquantifiable in 188 (26.1%). HBV RNA levels correlated moderately with HBV DNA levels in EP (ρ = 0.58, P = .01) and ENCH (ρ = 0.54, P < .001) and weakly in ENCI (ρ = 0.39, P < .001). HBsAg levels were only significantly correlated with HBV RNA levels in the ENCH group (ρ = -0.22, P = .05). In multivariable logistic regression, HBV RNA levels and HBV RNA to HBV DNA ratio were independently associated with significant liver fibrosis.

Conclusions: In our cohort of treatment-naive persons with HBV from Senegal, approximately 50% had undetectable HBV RNA levels. HBV RNA levels correlated with HBV DNA but not HBsAg levels in all phases of HBV infection and may provide an additional tool to assess HBV disease phase and activity.

Keywords: Africa; HBV RNA; biomarkers; hepatitis B virus; liver fibrosis.

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Conflict of interest statement

Potential conflicts of interest. L. B. reports support for travel and conference participation from the CROI foundation, and speaker honoraria from Roche, paid to his institution. G. W. received research grants from Gilead Sciences and honoraria for lectures and advisory boards from Roche Diagnostics, Gilead Sciences, MSD, and ViiV, all paid to his institution. A. R. reports support to his institution for advisory boards and/or travel grants from MSD, Gilead Sciences, Pfizer, and Moderna, and an investigator-initiated trial grant from Gilead Sciences, paid to his institution and outside the submitted work. A. R. M. reports travel support from Gilead Sciences, paid to his institution. G. W. received unrestricted research grants from Gilead Sciences and Roche Diagnostics, and lecture/advisory board membership fees from Gilead Sciences, MSD, and ViiV Healthcare, all paid to his institution. All other authors reported no potential conflicts of interest. All authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed.

Figures

Figure 1.
Figure 1.
Hepatitis B virus (HBV) RNA (A), quantitative hepatitis B surface antigen (B), and HBV DNA (C) levels in the different phases of HBV infection. Boxes show median and interquartile range (IQR), whiskers show outliers until 1.5× IQR, and circles show individual values of participants. P values describe pairwise comparisons between groups. Abbreviations: ENCH, hepatitis B e antigen–negative chronic hepatitis; ENCI, hepatitis B e antigen–negative chronic infection; EP, hepatitis B e antigen-positive; HBV, hepatitis B virus; qHBsAg, quantitative hepatitis B surface antigen.
Figure 2.
Figure 2.
Correlation between hepatitis B virus (HBV) RNA and HBV DNA (A, C, E) and between HBV RNA and quantitative hepatitis B surface antigen (B, D, F) in the different phases of HBV infection. Abbreviations: ENCH, hepatitis B e antigen–negative chronic hepatitis; ENCI, hepatitis B e antigen–negative chronic infection; EP, hepatitis B e antigen-positive; HBV, hepatitis B virus; qHBsAg, quantitative hepatitis B surface antigen.
Figure 3.
Figure 3.
Hepatitis B virus (HBV) DNA levels (A) and quantitative hepatitis B surface antigen levels (B) according to HBV RNA categories. Abbreviations: cp/mL, copies per milliliter; HBV, hepatitis B virus; LLOD, lower limit of detection; qHBsAg, quantitative hepatitis B surface antigen.
Figure 4.
Figure 4.
Univariable (blue) and multivariable (red) logistic regression models for factors associated with having at least significant liver fibrosis. Abbreviations: ALT, alanine aminotransferase; BMI, body mass index; HBeAg, hepatitis B e antigen; HBV, hepatitis B virus; qHBsAg, quantitative hepatitis B surface antigen.

References

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