Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 203, Issue 2, Pages 196-206Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jiq044
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Funding
- Ruth L. Kirschstein National Research Service Award [T32 AI007641-06A2]
- UCSF Liver Center [P30 DK026743]
- NIH/NCRR [UL1 RR024131]
- UCSF - GIVI Center for AIDS Research [P30 AI0277631]
- Harvey V. Berneking Living Trust
- NIH
- NIH Roadmap for Medical Research [DPI 0D00329]
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Background. Although the rate of mother-to-child transmission of hepatitis C virus (HCV) is low, the effect of HCV exposure in utero on the fetal immune system is unknown. Methods. Umbilical cord blood was obtained from 7 neonates born to HCV-seropositive, HCV RNA-positive women and 8 neonates born to HCV-seronegative women. Cord blood mononuclear cells were analyzed by immunophenotyping and by intracellular cytokine staining after HCV-specific and polyclonal stimulation. Plasma was analyzed for anti-HCV immunoglobulin M (IgM), cytokine/granzyme concentrations, and indoleamine 2,3-dioxygenase (IDO) activity. Results. HCV-exposed neonates had significantly lower levels of regulatory T cells expressing HLA-DR, lower CD4(+) and CD8(+) T cell activation, and lower plasma levels of pro-inflammatory markers than did controls. However, CD4(+) and CD8(+) T cells from HCV-exposed neonates had higher IFN-gamma production in response to polyclonal stimulation than did T cells from controls. IDO activity was similar between groups. No HCV-specific T cell responses or anti-HCV IgM were detected in any neonates. Conclusions. HCV-exposed neonates showed a relative suppression of immune activation and pro-inflammatory markers, which was counterbalanced by an increased production capacity for IFN-gamma. These results suggest that HCV encounters the fetal immune system in utero, and alters the balance between suppressive and pro-inflammatory responses.
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