Related Experiment Video
Updated: Aug 8, 2026
An In vitro Co-infection Model to Study Plasmodium falciparum-HIV-1 Interactions in Human Primary Monocyte-derived Immune Cells
Published on: August 15, 2012
Infection of human monocytes with HIV-1Ba-L. Effect on accessory cell function for T-cell proliferation in vitro
L M Melendez-Guerrero1, J K Nicholson, J S McDougal
1Department of Pathology, Emory University School of Medicine, Atlanta, GA.
Insights
Human immunodeficiency virus (HIV) infection impairs monocyte function, leading to reduced T-cell responses. HIV-infected monocytes release factors that suppress T-cell proliferation, contributing to immune dysfunction in AIDS.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Human immunodeficiency virus (HIV) infection and acquired immunodeficiency syndrome (AIDS) are characterized by altered CD4+ lymphocyte levels and diminished T-cell responses.
- Monocytes (M phi) play a crucial role in regulating T-cell proliferation.
Purpose of the Study:
- To investigate whether defective monocyte (M phi) function contributes to the impaired T-cell mitogenic responses observed in HIV infection.
- To determine the mechanism by which HIV-infected monocytes affect T-cell function.
Main Methods:
- Monocytes (M phi) were isolated from peripheral blood mononuclear cells (PBMC) of healthy donors.
- Isolated M phi were infected with the HIV-1 M phi-tropic strain, Ba-L.
- HIV-infected M phi were co-cultured with autologous T cells and T-cell mitogens to assess T-cell proliferation.
Main Results:
- T cells co-cultured with HIV-infected monocytes exhibited decreased proliferative responses to anti-CD3 monoclonal antibodies (Leu4, OKT3) and concanavalin A (Con A).
- Supernatants from HIV-infected M phi cultures, including heat-activated supernatants, suppressed the proliferative responses of normal PBMC.
- Inhibitors of HIV binding did not restore the proliferative capacity of HIV-infected cultures.
Conclusions:
- HIV infection of monocytes leads to the release of soluble factors that suppress T-cell proliferative responses.
- These soluble factors contribute to the impaired T-cell function observed in HIV-infected individuals.
Abstract:
Major laboratory manifestations of human immunodeficiency virus (HIV) infection and acquired immunodeficiency syndrome (AIDS) include altered levels of circulating CD4+ lymphocytes and decreased in vitro T-cell mitogenic responses. Since T-cell proliferation is regulated by monocytes (M phi), studies were undertaken to determine whether defective M phi function contributes to these poor mitogenic responses. M phi were isolated from peripheral blood mononuclear cells (PBMC) of normal donors by adherence to plastic. After 5 days in culture, the adherent cells were inoculated with the HIV-1 M phi-tropic strain, Ba-L. Under these conditions HIV infection in M phi can be detected 5-7 days after inoculation. Ten to fourteen days postinoculation, the adherent cells were harvested with lidocaine and cocultured with fresh autologous T cells and T-cell mitogens in a 3-day assay. We found decreased proliferative anti-CD3 responses to Leu4 and OKT3 and variable responses to concanavalin A (Con A) by T cells cultured with HIV-infected monocytes compared with T cells cultured with uninfected M phi. Supernatants from HIV-infected M phi cultures decreased proliferative responses of normal PBMC to anti-CD3 monoclonal antibodies. Heat-activated supernatants had the same effect. Inhibitors of HIV binding did not restore proliferative responses of HIV-infected cultures to normal levels. These results indicate that HIV infection of M phi causes the release of soluble factor(s) that suppress anti-CD3-induced T-cell proliferative responses.
