Abstract

Parvovirus B19 infection is a significant cause of fetal death. The aim of this study was to investigate the role of maternal immune status in modulating susceptibility to fetal B19 infection. Peripheral blood was obtained from pregnant women (n¼199) with no clinical evidence of recent B19 infection. Evaluation of ex vivo T cell responses from 149/199 individuals showed significantly higher interferon-g levels for seropositive individuals following VP1 (26836 versus 10319 pg/ml; P¼0.003)and VP2 (242 42 versus 9116 pg/ml; P¼0.01) antigen stimulation. Significantly higher levels of interleukin-2were also observed in seropositive individuals following both VP1 (P¼0.0003) and VP2 (P¼ 0.0005) stimulation. The observed Th1 cellular response is lower than that documented previously for non-pregnant individualsandstrongly suggests that diminution of the maternal antiviral immune response may increase susceptibility to fetal B19 infection.