Related Experiment Video
Updated: Jun 25, 2026

Isolation, Transfection, and Culture of Primary Human Monocytes
Published on: December 16, 2019
Lambda interferon inhibits human immunodeficiency virus type 1 infection of macrophages
1Division of Allergy & Immunology, The Children's Hospital of Philadelphia, University of Pennsylvania School of Medicine, 34th Street & Civic Center Boulevard, Philadelphia, PA 19104, USA.
Insights
Type III interferon (IFN-lambda) inhibits human immunodeficiency virus type 1 (HIV-1) replication in macrophages. This antiviral activity involves both extracellular and intracellular mechanisms, suggesting therapeutic potential for HIV-1 infection.
Area of Science:
- Immunology
- Virology
- Infectious Diseases
Background:
- Type III interferon (IFN-lambda) is a newly identified cytokine with broad-spectrum antiviral activity.
- Human immunodeficiency virus type 1 (HIV-1) infects macrophages, a critical cell type in viral replication and pathogenesis.
- Understanding novel antiviral mechanisms is crucial for developing effective HIV-1 therapies.
Purpose of the Study:
- To investigate the antiviral potential of type III interferon (IFN-lambda) against human immunodeficiency virus type 1 (HIV-1) in macrophages.
- To elucidate the mechanisms by which IFN-lambda inhibits HIV-1 infection and replication.
Main Methods:
- Blood monocyte-derived macrophages expressing IFN-lambda receptors were cultured.
- Macrophages were treated with IFN-lambda1 or IFN-lambda2 and subsequently infected with HIV-1.
- HIV-1 infection, replication, CCR5 expression, CC chemokine induction, and intracellular APOBEC3G/3F expression were analyzed.
Main Results:
- IFN-lambda1 and IFN-lambda2 significantly inhibited HIV-1 infection and replication in macrophages.
- The antiviral effect was observed against both laboratory-adapted and clinical HIV-1 strains.
- IFN-lambda induced CC chemokines and upregulated intracellular APOBEC3G/3F, while having minimal effect on CCR5 expression.
Conclusions:
- Type III interferon (IFN-lambda) possesses broad-spectrum anti-HIV-1 activity in macrophages.
- IFN-lambda inhibits HIV-1 replication through both extracellular (chemokine induction) and intracellular (APOBEC3G/3F upregulation) antiviral mechanisms.
- These findings highlight the therapeutic potential of IFN-lambda for treating HIV-1 infection.
Abstract:
The newly identified type III interferon (IFN-lambda) has antiviral activity against a broad spectrum of viruses. We thus examined whether IFN-lambda has the ability to inhibit human immunodeficiency virus type 1 (HIV-1) infection of blood monocyte-derived macrophages that expressed IFN-lambda receptors. Both IFN-lambda1 and IFN-lambda2, when added to macrophage cultures, inhibited HIV-1 infection and replication. This IFN-lambda-mediated anti-HIV-1 activity is broad, as IFN-lambda could inhibit infection by both laboratory-adapted and clinical strains of HIV-1. Investigations of the mechanism(s) responsible for the IFN-lambda action showed that although IFN-lambda had little effect on HIV-1 entry coreceptor CCR5 expression, IFN-lambda induced the expression of CC chemokines, the ligands for CCR5. In addition, IFN-lambda upregulated intracellular expression of type I IFNs and APOBEC3G/3F, the newly identified anti-HIV-1 cellular factors. These data provide direct and compelling evidence that IFN-lambda, through both extracellular and intracellular antiviral mechanisms, inhibits HIV-1 replication in macrophages. These findings indicate that IFN-lambda may have therapeutic value in the treatment of HIV-1 infection.
More Related Videos
Related Concept Videos
Inhibitors of Viral Protein Synthesis
Immune Response Against Viral Pathogens
NK Cells
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...
Inhibitors Of Virion Release
Inhibitors of Virion Maturation and Assembly

