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The impact of active HIV-1 replication on the physiological age-related decline of immature-transitional B-cells in HIV-1 infected children

Cagigi, Albertoa,*; Palma, Paolob,c,*; Nilsson, Annad,e; Di Cesare, Silviac; Pensieroso, Simoned; Kakoulidou, Mariaf; Bernardi, Stefaniac; Rossi, Paolob,c; Chiodi, Francescad

doi: 10.1097/QAD.0b013e32833c3298
Clinical Science: Concise Communications

Objective: To characterize the level of immature-transitional B-cells in blood during pediatric HIV-1 infection in relation to active or suppressed viremia. We also aimed at characterizing the level of expression of CXCR4, CXCR5 and CCR7 on immature-transitional B-cells, as these receptors are important mediators for homing of B-cells.

Design: Forty-eight HIV-1 vertically infected children (33 viral controllers and 15 viremic patients) and 33 age-matched healthy controls were enrolled in a cross-sectional study.

Methods: We measured the levels of peripheral immature-transitional B-cells in all groups in relation to switched memory B-cells by flow cytometry. In parallel we evaluated CXCR4, CXCR5 and CCR7 expression on immature-transitional B-cells and measured plasma levels of CXCL12, BAFF and interleukin-7 by ELISA.

Results: We observed a lack of physiological age-related decline of immature-transitional B-cells in viremic children in parallel to a decreased level of switched memory B-cells. Interestingly, immature-transitional B-cells from viremic children presented with high levels of CXCR4. On the contrary, the level of CXCL12, the natural ligand for CXCR4, was lowest in the HIV-1 infected group, as compared with controls.

Conclusion: Control of HIV-1 viremia through antiretroviral treatment appears to be crucial in decreasing the expansion and alteration of immature-transitional B-cells.

aDepartment of Laboratory Medicine, Division of Clinical Immunology, Karolinska University Hospital Huddinge, Stockholm, Sweden

bDivision of Immunology and Infectious Diseases, Ospedale Pediatrico ‘Bambino Gesù’, Italy

cChair of Pediatrics, Department of Public Health, University of Tor Vergata, Rome, Italy

dDepartment of Microbiology, Tumor and Cell Biology, Sweden

eDepartment of Women and Child Health, Karolinska Institutet, Sweden

fThe Swedish Institute for Infectious Disease Control, Stockholm, Sweden.

*First authorship shared.

Received 21 February, 2010

Revised 30 April, 2010

Accepted 14 May, 2010

Correspondence to Alberto Cagigi, PhD, Karolinska University Hospital Huddinge, Department of Laboratory Medicine, Division of Clinical Immunology, Alfred Nobels Allé 8, S 141 86 Stockholm, Sweden. E-mail:

© 2010 Lippincott Williams & Wilkins, Inc.