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

  1. Author:
    Moir, S.
    Malaspina, A.
    Ogwaro, K. M.
    Donoghue, E. T.
    Hallahan, C. W.
    Ehler, L. A.
    Liu, S. Y.
    Adelsberger, J.
    Lapointe, R.
    Hwu, P.
    Baseler, M.
    Orenstein, J. M.
    Chun, T. W.
    Mican, J. A. M.
    Fauci, A. S.

  2. Author Address

    NIAID, Immunoregulat Lab, NIH, Bldg 10, Room 6A02, Bethesda, MD 20892 USA. NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA. NCI, Surg Branch, NIH, Bethesda, MD 20892 USA. NCI, Frederick Canc & Dev Ctr, Sci Applicat Int Corp, Frederick, MD 21702 USA. George Washington Univ, Dept Pathol, Washington, DC 20037 USA. Moir S NIAID, Immunoregulat Lab, NIH, Bldg 10, Room 6A02, Bethesda, MD 20892 USA.
    1. Year: 2001
  2. Journal: Proceedings of the National Academy of Sciences of the United States of America
    1. 98
    2. 18
    3. Pages: 10362-10367
  4. Type of Article: Article
  1. 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.

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