## Abstract Over 90% of infants infected with hepatitis B virus (HBV) caused by motherβtoβinfant transmission will evolve to carrier status, and this cannot be prevented until widespread administration of the HB vaccine and hepatitis B immune globulin (HBIG) is implemented. This prospective study o
Cellular Immune Response to HBcAg in Mother-to-Infant Transmission of Hepatitis B Virus
β Scribed by Hong-Yuan Hsu; Mei-Hwei Chang; Kue-Hsiung Hsieh; Chin-Yun Lee; Ho-Hsiung Lin; Lih-Hwa Hwang; Pei-Jer Chen; Ding-Shinn Chen
- Publisher
- John Wiley and Sons
- Year
- 1992
- Tongue
- English
- Weight
- 800 KB
- Volume
- 15
- Category
- Article
- ISSN
- 0270-9139
No coin nor oath required. For personal study only.
β¦ Synopsis
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 HBeAgpositive 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 HBcAg 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.)
The outcome of HBV infection is determined by the interaction between host immune system and virus (1). Exposure to HBV in the perinatal period, as in neonates born to HBeAg-positive carrier mothers, frequently
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