Age, race and viral genotype are associated with the prevalence of hepatitis B e antigen in children and adults with chronic hepatitis B

the Hepatitis B Research Network (HBRN)

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

Hepatitis B e antigen (HBeAg) is an important serological marker of hepatitis B virus (HBV) infection and is associated with higher levels of viraemia, increased risk of infectivity to others and increased risk of hepatocellular carcinoma. We analysed HBeAg status in a large cohort of adults and children enrolled in Cohort Studies of the Hepatitis B Research Network, long-term natural history studies of chronic HBV infection. A cross-sectional analysis examined factors associated with HBeAg positivity, including demographic and virologic data, across the age spectrum. Among 2241 enrolled participants who met criteria for this analysis, 825 (37%) were seropositive for HBeAg. The prevalence of HBeAg was lower in those with older age, ranging from 85% among those up to 10 years of age to only 12% among those older than 50 years. In addition to age, both race and HBV genotype were independently associated with HBeAg positivity. There was a significant interaction between age and race; the prevalence of HBeAg was significantly higher among Asians > 10-30 years old vs Whites or Blacks who were >10 to 30 years old and those infected with HBV genotype C. Conversely, the presence of the basal core promoter and precore variants was associated with significantly lower prevalence of HBeAg, even when adjusted for age, race and genotype. These data will provide a better understanding of factors associated with seropositivity for HBeAg and may lead to better strategies for preventing HBV infection and broader indications for antiviral therapy.

Original languageEnglish (US)
Pages (from-to)856-865
Number of pages10
JournalJournal of Viral Hepatitis
Volume26
Issue number7
DOIs
StatePublished - Jul 2019

Bibliographical note

Funding Information:
Funding information The HBRN was funded as a Cooperative Agreement between the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) to the following investigators: Lewis R. Roberts, MB, ChB, PhD (U01-DK082843); Anna Suk-Fong Lok, MD (U01-DK082863); Steven H. Belle, PhD, MScHyg (U01-DK082864); Kyong-Mi Chang, MD (U01-DK082866); Michael W. Fried, MD (U01-DK082867); Adrian M. Di Bisceglie, MD (U01-DK082871); William M. Lee, MD (U01-DK082872); Harry L. A. Janssen, MD, PhD (U01-DK082874); Daryl T-Y Lau, MD, MPH (U01-DK082919); Richard K. Sterling, MD, MSc (U01-DK082923);Steven-Huy B. Han, MD (U01-DK082927); Robert C. Carithers, MD (U01-DK082943); Norah A. Terrault, MD, MPH (U01-DK082944); and Kathleen B. Schwarz, MD (U01-DK082916), an interagency agreement with NIDDK: Lilia M. Ganova-Raeva, PhD (A-DK-3002-001), and support from the intramural programme, NIDDK, NIH: Marc G. Ghany, MD. Additional funding to support this study was provided to Kyong-Mi Chang, MD, the Immunology Center (NIH/NIDDK Center of Molecular Studies in Digestive and Liver Diseases P30DK50306, NIH Public Health Service Research Grant M01-RR00040), Richard K. Sterling, MD, MSc (UL1TR000058, NCATS (National Center for Advancing Translational Sciences, NIH)), Norah A. Terrault, MD, MPH (CTSA Grant Number UL1TR000004), Michael W. Fried, MD (CTSA Grant Number UL1TR001111), Anna Suk-Fong Lok (CTSA Grant Number UL1RR024986, U54TR001959) and Kathleen B. Schwarz, MD (CTSA Grant Number UL1TR000423). Additional support was provided by Gilead Sciences, Inc, and Roche Molecular Systems via a CRADA through the NIDDK. The investigators wish to acknowledge the support provided via CRADAs through the NIDDK by Gilead Sciences, Inc., and Roche Molecular Systems. The investigators recognize and appreciate the contributions of the HBRN participants without whom this research would not be possible.

Funding Information:
The investigators wish to acknowledge the support provided via CRADAs through the NIDDK by Gilead Sciences, Inc., and Roche Molecular Systems. The investigators recognize and appreciate the contributions of the HBRN participants without whom this research would not be possible.

Funding Information:
PhD (U01‐DK082874); Daryl T‐Y Lau, MD, MPH (U01‐DK082919); Richard K. Sterling, MD, MSc (U01‐DK082923);Steven‐Huy B. Han, MD (U01‐DK082927); Robert C. Carithers, MD (U01‐DK082943); Norah A. Terrault, MD, MPH (U01‐DK082944); and Kathleen B. Schwarz, MD (U01‐DK082916), an interagency agreement with NIDDK: Lilia M. Ganova‐Raeva, PhD (A‐DK‐3002‐001), and support from the intramural programme, NIDDK, NIH: Marc G. Ghany, MD. Additional funding to support this study was provided to Kyong‐Mi Chang, MD, the Immunology Center (NIH/NIDDK Center of Molecular Studies in Digestive and Liver Diseases P30DK50306, NIH Public Health Service Research Grant M01‐ RR00040), Richard K. Sterling, MD, MSc (UL1TR000058, NCATS (National Center for Advancing Translational Sciences, NIH)), Norah A. Terrault, MD, MPH (CTSA Grant Number UL1TR000004), Michael W. Fried, MD (CTSA Grant Number UL1TR001111), Anna Suk‐Fong Lok (CTSA Grant Number UL1RR024986, U54TR001959) and Kathleen B. Schwarz, MD (CTSA Grant Number UL1TR000423). Additional support was provided by Gilead Sciences, Inc, and Roche Molecular Systems via a CRADA through the NIDDK.

Publisher Copyright:
© 2019 John Wiley & Sons Ltd

Keywords

  • e antigen
  • hepatitis B
  • natural history

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