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PMID: 11504927 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S.

HIV-1 induces phenotypic and functional perturbations of B cells in chronically infected individuals.

Proceedings of the National Academy of Sciences of the United States of America ·Vol. 98 ·No. 18 ·2001-08-28 ·Pages 10362-7

Moir S, Malaspina A, Ogwaro KM, Donoghue ET, Hallahan CW, Ehler LA, Liu S, Adelsberger J, Lapointe R, Hwu P, Baseler M, Orenstein JM, Chun TW, Mican JA, Fauci AS

Abstract

A number of perturbations of B cells has been described in the setting of HIV infection; however, most remain poorly understood. To directly address the effect of HIV replication on B cell function, we investigated the capacity of B cells isolated from HIV-infected patients to respond to a variety of stimuli before and after reduction of viremia by effective antiretroviral therapy. B cells taken from patients with high levels of plasma viremia were defective in their proliferative responses to various stimuli. Viremia was also associated with the appearance of a subpopulation of B cells that expressed reduced levels of CD21. After fractionation into CD21(high)- and CD21(low)-expressing B cells, the CD21(low) fraction showed dramatically reduced proliferation in response to B cell stimuli and enhanced secretion of immunoglobulins when compared with the CD21(high) fraction. Electron microscopic analysis of each fraction revealed cells with plasmacytoid features in the CD21(low) B cell population but not in the CD21(high) fraction. These results indicate that HIV viremia induces the appearance of a subset of B cells whose function is impaired and which may be responsible for the hypergammaglobulinemia associated with HIV disease.

MeSH Terms
Antigens, CD19/genetics,metabolism B-Lymphocyte Subsets/immunology,ultrastructure B-Lymphocytes/immunology,ultrastructure Base Sequence DNA Primers/genetics Gene Expression HIV Infections/genetics,immunology HIV-1/pathogenicity Humans Hypergammaglobulinemia/etiology Immunophenotyping Lymphocyte Activation Microscopy, Electron Receptors, Complement 3d/genetics,metabolism Viremia/genetics,immunology
Chemicals
Antigens, CD19 DNA Primers Receptors, Complement 3d
Authors & Affiliations
15 authors, click to expand affiliations / ORCID
Moir S
Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, and Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. smoir@niaid.nih.gov
Malaspina A
Ogwaro K M
Donoghue E T
Hallahan C W
Ehler L A
Liu S
Adelsberger J
Lapointe R
Hwu P
Baseler M
Orenstein J M
Chun T W
Mican J A
Fauci A S
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Article Info
Journal
Proceedings of the National Academy of Sciences of the United States of America
Abbr.
Proc Natl Acad Sci U S A
ISSN
0027-8424
DOI
10.1073/pnas.181347898
Email
smoir@niaid.nih.gov
Published
2001-08-28
Epub
2001-00-14
Pages
10362-7
Language
English
Region
United States
NLM ID
7505876
PMCID
PMC56966
Subset
IM
Grants
NCI NIH HHS · N01-CO-56000 · United States
External Links
PubMed source DOI: 10.1073/pnas.181347898 PMC Full Text View journal details
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