The hepatitis B virus e antigen suppresses the respiratory burst and mobility of human monocytes and neutrophils

Chuen Miin Leu*, Yong Chen Lu, Wei Li Peng, Hsin Tzu Chu, Cheng po Hu

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

16 Scopus citations


The Hepatitis B virus (HBV) e antigen (HBeAg) is a secretory, non-structural protein, and associated with persistent infection of HBV. Previous studies indicate that HBeAg is able to regulate T cell-mediated responses, however, the interaction between HBeAg and the innate immune system is poorly understood. In this study, we demonstrated that recombinant HBeAg (rHBe) bound to human peripheral blood monocytes, neutrophils, and B lymphocytes but not to T lymphocytes. We focused on investigating the effects of HBeAg on monocytes and neutrophils and found that rHBe decreased the respiratory burst in both types of cells. Furthermore, we observed that cell migration in monocytes and neutrophils was suppressed by rHBe in a transwell assay. The attenuation of rHBe was not caused by a general cytotoxic effect because rHBe treatment stimulated low levels of cytokine and chemokine production by monocytes and it promoted neutrophil survival. Since the recruitment of monocytes and neutrophils to the infected site is crucial for the initiation of inflammation, HBeAg may modulate innate immune responses by diminishing the respiratory burst and migration of monocytes and neutrophils, which might interfere with the subsequent innate and adaptive immune responses against HBV, leading to the establishment of chronic infection.

Original languageEnglish
Pages (from-to)880-887
Number of pages8
Issue number11
StatePublished - 1 Nov 2014


  • Chemokinesis
  • Hepatitis B virus e antigen
  • Innate immune response
  • Monocytes
  • Neutrophils
  • Respiratory burst


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