Cellular Immune Response to HBcAg in Mother‐to‐Infant Transmission of Hepatitis B Virus

Cellular immunity to HBcAg was studied in hepatitis B virus carrier children and neonates born to hepatitis B virus carrier mothers. A significant proliferative response of peripheral blood mononuclear cells to HBcAg was found in 5 of 10 children with elevated ALT levels but in none of the nine HBeAg‐positive children with normal ALT levels. HBeAg but not HBsAg was detected in cord blood of 9 of 10 neonates born to HBeAg‐positive carrier mothers, suggesting exposure of these neonates to HBeAg in utero. However, cord mononuclear cells from neonates born to HBeAg‐positive carrier mothers did not show a significant change in the proportion of suppressor and helper T‐cell subsets or proliferative response to HBcAg. Nor did they produce interleukin‐2 receptor after being cocultured with HBcAg. The unresponsiveness of peripheral‐blood mononuclear cells or cord mononuclear cells to HBeAg was not reversed by CD8⁺ cell depletion. Although cord blood mononuclear cells from neonates born to carrier mothers positive for antibody to HBeAg also did not respond to HBcAg, we encountered an infant, born to a carrier mother positive for antibody to HBeAg, who contracted acute hepatitis B at 2.5 mo of age. The baby's peripheral‐blood mononuclear cells showed a significant proliferative response to HBcAg. These results support the view that transplacental maternal HBeAg probably induces a specific unresponsiveness of helper T cells to HBcAg and HBeAg in the neonates born to HBeAg‐positive carrier mothers. This specific helper T cell tolerance could be maintained throughout the early replicative phase of carrier state but might break someday with the appearance of raised ALT level. (HEPATOLOGY 1992;15:770–776).