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Circulating memory B-cell subpopulations are affected differently by HIV infection and antiretroviral therapy

D'Orsogna, Lloyd Ja; Krueger, Rom Gb; McKinnon, Elizabeth Jc; French, Martyn Aa,d

doi: 10.1097/QAD.0b013e32828642c7
Clinical Science

Objective: To determine if the depletion of IgM memory B cells might contribute to the increased susceptibility of HIV patients to pneumococcal infection, memory B-cell subpopulations were investigated in HIV patients, including patients receiving antiretroviral therapy (ART).

Methods: Blood B cells with the phenotype of IgM memory B cells (CD27+, IgM+) and switched memory B cells (CD27+, IgM) were measured in antiretroviral-treated (n = 32) and untreated (n = 24) HIV patients and non-HIV controls (n = 35). Serum levels of IgG and IgG2 antibodies to pneumococcal polysaccharides, IgG, IgG subclasses, IgM and IgA were also assayed in HIV patients.

Results: Switched memory B-cell counts were lower than controls in HIV patients (P < 0.01) irrespective of antiretroviral status and correlated with CD4 T-cell counts (r = 0.56, P = 0.001) in treated patients. In untreated patients, IgM memory B-cell counts correlated with CD4 T-cell counts (r = 0.73, P < 0.0001) reflecting higher values than controls in patients with CD4 T-cell counts greater than 300 cells/μl (P = 0.004) and lower values than controls in patients with CD4 T-cell counts below 300 cells/μl (P = 0.0001). There was no relationship between serum levels of pneumococcal antibodies and IgM or switched memory B cells.

Conclusion: The depletion of IgM memory B cells in untreated HIV patients with a CD4 T-cell count below 300 cells/μl might be a risk factor for pneumococcal infection. The depletion of switched memory B cells is a complication of HIV infection irrespective of ART and might contribute to impaired IgG antibody responses. Memory B-cell subpopulations might predict the risk of pneumococcal sepsis more accurately than the CD4 T-cell count or pneumococcal antibody levels.

From the aDepartment of Clinical Immunology and Immunogenetics, Royal Perth Hospital, Perth, Australia

bFlow Cytometry Unit, Core Services Laboratory, Royal Perth Hospital, Perth, Australia

cCentre for Clinical Immunology and Biomedical Statistics, Murdoch University, Perth, Australia

dSchool of Surgery and Pathology, University of Western Australia, Perth, Australia.

Received 16 November, 2006

Revised 16 May, 2007

Accepted 22 May, 2007

Correspondence to Martyn French, Department of Clinical Immunology and Immunogenetics, Royal Perth Hospital, GPO Box X2213, Perth, WA 6847, Australia. E-mail: martyn.french@health.wa.gov.au

© 2007 Lippincott Williams & Wilkins, Inc.