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In Vitro Assay to Evaluate the Impact of Immunoregulatory Pathways on HIV-specific CD4 T Cell Effector Function
Published on: October 16, 2013
Modulation of human immunodeficiency virus type 1 infection of human monocytes by IgA
E N Janoff1, S M Wahl, K Thomas
1Department of Medicine, VA Medical Center, Minneapolis, MN 55417, USA.
Insights
Immunoglobulin A (IgA) from HIV-1 patients can enhance HIV-1 infection of monocytes. This IgA-mediated enhancement suggests a complex role for the immune system in HIV-1 pathogenesis.
Area of Science:
- Immunology
- Virology
- Infectious Diseases
Background:
- Human immunodeficiency virus type 1 (HIV-1) infection primarily targets CD4+ T cells, but also infects monocytes and macrophages.
- The role of immunoglobulin A (IgA) in HIV-1 infection is not fully understood, with potential roles in both protection and enhancement.
Purpose of the Study:
- To investigate the effect of serum IgA from HIV-1-infected patients on the in vitro infection of primary human blood monocytes by the monocyte-tropic HIV-1Bal strain.
- To explore whether IgA-mediated enhancement of HIV-1 infection extends to other relevant cell types, such as intestinal mononuclear cells.
Main Methods:
- Purified serum IgA from HIV-1-infected patients and seronegative controls was preincubated with HIV-1Bal.
- The virus-IgA mixture was used to infect primary human blood monocytes.
- Reverse transcriptase activity was measured to quantify viral replication.
- Monocytes were preincubated with nonimmune IgA to assess the role of Fc alpha receptors.
- Experiments were repeated with human mononuclear cells from the intestinal lamina propria.
Main Results:
- Preincubation of HIV-1Bal with serum IgA from 6 out of 14 HIV-1-infected patients significantly increased viral reverse transcriptase activity (>50%) compared to controls.
- This enhancement was observed regardless of the patient's CD4 T cell count or clinical stage.
- The IgA-mediated enhancement of HIV-1 infection was inhibited by preincubating monocytes with nonimmune IgA, suggesting Fc alpha receptor involvement.
- Similar enhancement was observed with mononuclear cells from the intestinal lamina propria.
Conclusions:
- Serum IgA from some HIV-1-infected individuals can enhance the infection of monocytes and intestinal mononuclear cells by HIV-1.
- This IgA-mediated enhancement may contribute to HIV-1 pathogenesis in both circulating monocytes and mucosal macrophages.
- Further research is needed to elucidate the complex role of IgA and the mucosal immune system in HIV-1 infection and disease progression.
Abstract:
The effect of IgA from human immunodeficiency virus type 1 (HIV-1)-infected patients on infection of primary human blood monocytes with the monocyte-tropic strain HIV-1Bal was evaluated in vitro. Preincubation of HIV-1Bal with purified serum IgA from 6 of 14 patients but from none of 5 seronegative subjects caused a > 50% increase in reverse transcriptase activity. This increase was inhibited by preincubation of monocytes with nonimmune IgA, suggesting a role for Fc alpha receptors. Results were independent of CD4 T cell number and clinical stage. The IgA-mediated enhancement extended to more biologically relevant human mononuclear cells isolated from the intestinal lamina propria. The ability of serum IgA to enhance HIV-1 infection may be relevant to infection of both circulating monocytes and mucosal macrophages. These studies suggest the need to characterize the complex contribution of IgA and the mucosal immune system in promoting and preventing primary HIV-1 infection.
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