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Original Article

Antibodies against pneumococcal capsular polysaccharide in Malawian HIV-positive mothers and their HIV-exposed uninfected children

, , , , , , , , & show all
Pages 317-321 | Received 24 Jul 2015, Accepted 23 Oct 2015, Published online: 26 Nov 2015
 

Abstract

Background HIV-exposed uninfected children have a higher risk of infection and mortality compared to HIV-unexposed children and the reasons for this vulnerability are still under investigation. Aim: This study aimed to evaluate the influence of maternal HIV parameters on the passive transfer of anti-pneumococcal capsular polysaccharide (PCP) IgG and to determine whether the concentrations of specific IgG might be related to the morbidity and mortality in HIV-exposed uninfected children. Methods One hundred and twenty-six Malawian HIV-infected pregnant women and their uninfected children were studied. Antiretroviral treatment-naive women started a nevirapine-based triple combination regimen from the third trimester of pregnancy until at least 6 months of exclusive breastfeeding. Mother/child pairs were followed until 2 years after delivery. Plasma anti-PCP IgG titers (in mothers at 26 weeks of gestation and in infants at 1 and 6 months) were determined by an enzyme-linked immunosorbent assay. None of these women and children had received any vaccination against pneumococcal polysaccharides. Results Maternal anti-PCP IgG concentration was independent from viral load (p = 0.848), CD4 count (p = 0.740) and WHO stage (p = 0.450). However, the child/mother ratio of anti-PCP IgG measured at 1 month among infants was significantly reduced in pairs whose mothers had HIV-RNA > 10 000 copies/ml (p = 0.043) and CD4 < 350 cells/μl (p = 0.090) before antiretroviral therapy (ART). No clear associations between anti-PCP IgG and respiratory-related deaths were found, but respiratory infection episodes were more frequent among children with lower anti-PCP IgG ratio (p = 0.046). Conclusion This study indicates that HIV pre-ART conditions in mothers may influence the rate of specific immunoglobulins transfer, increasing infants vulnerability to respiratory infections.

Acknowledgements

We thank Alessandra Mattei for providing secretarial help, Tonino Sofia for providing comments and help in the revision of the final manuscript, Marco Mirra, Massimiliano Di Gregorio, Stefano Lucattini and Luca Fucili for IT support and Ferdinando Costa and Patrizia Cocco for technical support.

Disclosure statement

All other authors report no conflicts of interest.

Funding information

This work was supported by funds from Istituto Superiore di Sanità Rome, Italy (Grant N. 528c/28c7); by a grant from the Italian Research Program on AIDS of the Ministry of Health 2009–2010 (N. 3H/33); and by Esher-Italy, Ministry of Health 2009–2010 (Grant N. 9M34). No funding was received for this work from any of the following organizations: National Institutes of Health (NIH); Wellcome Trust; and the Howard Hughes Medical Institute (HHMI). Stefano Vella has received honoraria from ViiV, Gilead and Merck for scientific board membership.

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