Related Experiment Video
Updated: May 6, 2026

A Restriction Enzyme Based Cloning Method to Assess the In vitro Replication Capacity of HIV-1 Subtype C Gag-MJ4 Chimeric Viruses
Published on: August 31, 2014
APOBEC3G and APOBEC3F require an endogenous cofactor to block HIV-1 replication
Yanxing Han1, Xiaojun Wang, Ying Dang
1Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan, United States of America.
APOBEC3G (A3G) and APOBEC3F (A3F) normally inhibit HIV-1, but not in CEM-T4 cells. These cells lack a crucial cofactor for A3G/A3F antiviral activity, revealing a new target for HIV-1 research.
Area of Science:
- Virology
- Molecular Biology
- Immunology
Background:
- APOBEC3G (A3G) and APOBEC3F (A3F) are cytidine deaminases that inhibit HIV-1 replication.
- Their precise anti-HIV mechanisms, including interactions with cellular proteins, remain incompletely understood.
- Previous studies suggested A3G/A3F disrupt viral reverse transcription or integration.
Purpose of the Study:
- To investigate the anti-HIV activity of endogenous APOBEC3G (A3G) and APOBEC3F (A3F) in different human T cell lines.
- To identify factors contributing to the loss of A3G/A3F antiviral function in specific cell lines.
- To elucidate the cellular requirements for A3G/A3F-mediated restriction of HIV-1.
Main Methods:
- Infection of six human T cell lines with wild-type and vif-deficient HIV-1.
- Analysis of A3G/A3F protein expression and function in CEM-T4 cells.
- Overexpression of exogenous A3G/A3F in CEM-T4 cells.
- Formation of heterokaryons by fusing CEM-T4 cells with 293T cells.
Main Results:
- CEM-T4 cells, despite high endogenous A3G/A3F levels, showed no restriction of vif-deficient HIV-1.
- Endogenous A3G/A3F genes in CEM-T4 cells were mutation-free and functionally normal.
- Overexpressed A3G/A3F failed to restore anti-HIV activity in CEM-T4 cells.
- Fusion of CEM-T4 cells with 293T cells restored A3G/A3F antiviral activity.
Conclusions:
- CEM-T4 cells possess functionally normal A3G/A3F but lack a critical cellular cofactor necessary for their anti-HIV activity.
- The identified cofactor is essential for A3G/A3F-mediated restriction of HIV-1 replication.
- Further research into this cofactor may offer novel therapeutic strategies against HIV-1.
More Related Videos
07:22A High-throughput Cre-Lox Activated Viral Membrane Fusion Assay to Identify Inhibitors of HIV-1 Viral Membrane Fusion
Published on: August 14, 2018
13:07Determining 3'-Termini and Sequences of Nascent Single-Stranded Viral DNA Molecules during HIV-1 Reverse Transcription in Infected Cells
Published on: January 30, 2019
Related Concept Videos
Retrovirus Life Cycles
Retroviruses
Eukaryotic Transcription Inhibitors
Eukaryotic transcription inhibitors usually contain two distinct domains, a...
Cofactors and Coenzymes
Cofactors can be metallic ions or organic molecules called coenzymes. These types of helper...
Inhibitors of Bacterial DNA Synthesis
Inhibitors of Viral Protein Synthesis