Objectives: Placental antibody transfer is impaired in the context of HIV infection, which may render HIV-exposed, uninfected infants vulnerable to group B Streptococcus (GBS) disease. The GBS antibody response predominately consists of immunoglobulin G2 (IgG2) antibody. Thus we determined whether concentration and placental transfer of anti-GBS antibody subclasses was altered in HIV-infected compared with HIV-uninfected mothers. Design: A retrospective analysis of anti-GBS antibody subclasses in 38 HIV-infected and 33 HIV-uninfected mothers and their uninfected infants. Methods: Sera were analysed using a novel flow cytometric assay that quantified binding of IgG1, IgG2, IgG3 and IgG4 to serotype (ST)Ia, STIII and STV GBS bacteria. Results: IgG2 binding to GBS STIa and V was lower in HIV-infected women compared with HIV-uninfected women. Moreover, IgG2 binding to GBS STIa was also lower in HIV-exposed, uninfected infants compared with unexposed infants. However, there were no statistically significant differences in the transplacental transfer ratio of IgG2 for any GBS serotype. The transplacental transfer of total IgG was reduced for GBS STIII and V and IgG1 subclass for STIII; placental transfer of all other subclasses was comparable in HIV-affected and HIV-unaffected pregnancies. Conclusion: Anti-GBS IgG2 placental transfer is not affected by HIV infection. This is important for functional antibody against the capsular polysaccharide of GBS and provides confidence that maternal GBS vaccination may result in functional activity in HIV-infected and uninfected women.
Bibliographical noteFunding Information:
We thank the mothers and infants who participated in this study, Prof. Carol Baker for the donation of positive control sera and Prof. Androulla Efstraitou for supplying the GBS clinical isolates. Contribution statement: K.L.D. developed the manuscript and original research idea. A.H., P.H., B.K., A.G., L.A., S.T. and C.J. developed the original idea and substantially contributed to the development of the manuscript. Funding: K.L.D. is supported by a Wellcome Trust Clinical Research Training Fellowship (KLD2013) The Thomas Watt Eden Fellowship (Royal College of Physicians Grant Number 01012013); and the Gilead/ BHIVA Registrar Award. B.K. is supported by the MRC (MR/K007602/1, MC-UP-A900/1122). C.J. was supported by the European Society for Pediatric Infectious Diseases and the Thrasher Research Fund.
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- Group B Streptococcus