Mediators of Fusion between HIV-Infected Macrophages and Lymphoid Cells

  • Suzanne Crowe
  • John Mills
  • Michael S. McGrath
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 300)


Shortly after the discovery of the human immunodeficiency virus (HIV) and recognition that it was the causative agent of the acquired immunodeficiency syndrome (AIDS), the CD4 molecule was identified as the principal receptor for the virus by Dalgleish and Klatzmann and their collaborators (1,2).The CD4 molecule is a member of the immunoglobulin superfamily, and was originally recognized as a surface marker for the helper-inducer T lymphocyte subset (3).However, other cells are known to express CD4, including follicular dendritic cells and cells of the monocyte-macrophage series (4,5,6). It was thus not surprising that by 1987 several groups had shown that monocyte-macrophages were susceptible to HIV infection(6-8). Infection of normal monocyte-macrophages cultured in vitro with laboratory strains of HIV resulted either in no infection whatsoever (as is characteristic of the HTLV-IIIB strain of HIV (6,8)),or in infection of up to 70% of the cultured cells (6-8). HIV infection of monocyte macrophages has very different characteristics than infection of peripheral blood lymphocytes or lymphoid cells. Replication of the virus was comparatively delayed, with peak titers of virus and viral products being reached many days or weeks after infection (6). Although some viral cytopathology was induced, primarily multinucleate giant cell formation, the infected cells survived in culture and continued to produce virus for periods of up to several months (6-8,9). These properties of the in vitro infection have led several investigators to hypothesize that long-lived tissue macrophages might serve as a reservoir for HIV infection in vivo (6,9).Certainly a reservoir of virus replication other than CD4 lymphocytes must exist, as recent studies have shown that patients with HIV infection develop progressively increasing titers of virus in plasma with time, as the CD4 lymphocyte count falls inexorably toward virtually undetectable levels (10,11). Tissue monocyte-macrophages are certainly a possible source for this virus, as advanced HIV infection is not associated with marked reduction in circulating or tissue monocyte-macrophage numbers (12 and Crowe SM, unpublished data).


Human Immunodeficiency Virus Human Immunodeficiency Virus Type Human Immunodeficiency Virus Infection Lymphoid Cell Infected Macrophage 
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Copyright information

© Plenum Press, New York 1991

Authors and Affiliations

  • Suzanne Crowe
    • 1
  • John Mills
    • 2
    • 3
  • Michael S. McGrath
    • 2
  1. 1.MacFarlane Burnet Centre for Medical ResearchFairfieldAustralia
  2. 2.Medical ServiceSan Francisco General HospitalUSA
  3. 3.Departments of Medicine, Microbiology and Laboratory MedicineUniversity of CaliforniaSan FranciscoUSA

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