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Related Experiment Videos

CD4+ lymphocyte function with early human immunodeficiency virus infection.

R J Gurley1, K Ikeuchi, R A Byrn

  • 1New England Deaconess Hospital, Division of Hematology/Oncology, Harvard Medical School, Boston, MA.

Proceedings of the National Academy of Sciences of the United States of America
|March 1, 1989
PubMed
Summary
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Human immunodeficiency virus (HIV) infection impairs T-cell antigen recognition in patients with acquired immunodeficiency syndrome-related complex (ARC). This defect is linked to HIV envelope gp120, not CD4+ cell loss.

Area of Science:

  • Immunology
  • Virology
  • Cellular Biology

Background:

  • Cellular immune deficiency in human immunodeficiency virus (HIV) infection may stem from CD4+ lymphocyte dysfunction.
  • Understanding T-cell responses to antigens is crucial for characterizing HIV pathogenesis.

Purpose of the Study:

  • To investigate T-lymphocyte responses to soluble antigens in HIV-infected individuals, including those with acquired immunodeficiency syndrome-related complex (ARC).
  • To determine the impact of HIV envelope protein gp120 and soluble CD4 on T-cell function.

Main Methods:

  • Isolated peripheral blood lymphocytes (PBLs) and CD4+ lymphocytes from healthy HIV-negative controls, asymptomatic HIV-positive subjects, and ARC patients.
  • Assessed T-lymphocyte proliferation in response to mitogens (phytohemagglutinin, PMA, calcium ionophore), tetanus toxoid, and recombinant HIV envelope gp120.

Related Experiment Videos

  • Evaluated the effect of recombinant gp120 and soluble CD4 on T-cell responses.

    • Main Results:

    • Asymptomatic HIV-infected subjects showed normal T-cell proliferation to mitogens and tetanus toxoid.
    • ARC patients exhibited a selective antigen recognition defect, independent of CD4+ cell counts.
    • Recombinant gp120 inhibited CD4+ lymphocyte proliferation to tetanus toxoid by 30-40%, suggesting an impact on MHC II-restricted antigen recognition.
    • Soluble CD4 did not affect T-cell responses to antigen.

    Conclusions:

    • A selective antigen recognition defect emerges in subjects with ARC, not early in HIV infection.
    • HIV's gp120 may impair T-cell recognition of antigens via major histocompatibility complex II, irrespective of CD4+ T-cell depletion.
    • This suggests a qualitative defect in T-cell function contributing to immune deficiency in HIV/AIDS.