Hepatitis B virus surface antigen suppresses the activation of monocytes through interaction with a serum protein and a monocyte-specific receptor

J Gen Virol. 2002 Jun;83(Pt 6):1281-1289. doi: 10.1099/0022-1317-83-6-1281.

Abstract

During hepatitis B virus (HBV) infection, high numbers of non-infectious HBV surface antigen (HBsAg) particles are present in circulation. It is shown here that recombinant HBsAg (rHBsAg) particles, which contain the S protein only, bind almost exclusively to monocytes. Attachment of rHBsAg to the THP-1 pre-monocytic cell line occurs upon 1,25-dihydroxyvitamin D3-induced differentiation. Binding to monocytes is enhanced by a heat-labile serum protein and is inhibited by Ca(2+)/Mg(2+), low pH and an HBsAg-specific monoclonal antibody. Furthermore, it is shown that rHBsAg suppresses lipopolysaccharide- and IL-2-induced production of cytokines. These results suggest the existence of a monocyte-specific receptor, the engagement of which by HBsAg suppresses the activity of these cells.

MeSH terms

  • Antibodies, Monoclonal / pharmacology
  • Blood Proteins / pharmacology
  • Calcitriol
  • Calcium / pharmacology
  • Cell Differentiation
  • Cells, Cultured
  • Cytokines / analysis
  • Dose-Response Relationship, Drug
  • Hepatitis B Surface Antigens / immunology*
  • Hot Temperature
  • Humans
  • Hydrogen-Ion Concentration
  • Interleukin-2
  • Lipopolysaccharide Receptors / metabolism
  • Lipopolysaccharides
  • Magnesium / pharmacology
  • Monocytes / immunology*
  • Monocytes / metabolism
  • Protein Binding / drug effects
  • Recombinant Proteins / immunology

Substances

  • Antibodies, Monoclonal
  • Blood Proteins
  • Cytokines
  • Hepatitis B Surface Antigens
  • Interleukin-2
  • Lipopolysaccharide Receptors
  • Lipopolysaccharides
  • Recombinant Proteins
  • Calcitriol
  • Magnesium
  • Calcium