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Published on: August 14, 2018
Different interaction between HIV-1 Vif and its cellular target proteins APOBEC3G/APOBEC3F
Tamiko Nagao1, Tomoki Yamashita, Ariko Miyake
1Department of Microbiology, Institute of Health Biosciences, University of Tokushima Graduate School, Tokushima, Japan.
The Journal of Medical Investigation : JMI
|March 20, 2010
Summary
Human immunodeficiency virus type 1 (HIV-1) Vif protein mutants unable to grow in cells failed to counteract APOBEC3G/APOBEC3F. Vif
Area of Science:
- Virology
- Molecular Biology
- Immunology
Background:
- The human immunodeficiency virus type 1 (HIV-1) Vif protein is crucial for viral replication.
- Cellular proteins APOBEC3G and APOBEC3F are potent restriction factors that inhibit HIV-1 replication.
- Vif antagonizes APOBEC3G/APOBEC3F, enabling efficient viral spread.
Purpose of the Study:
- To investigate the interaction between HIV-1 Vif mutants and APOBEC3G/APOBEC3F.
- To determine the functional domains of Vif responsible for counteracting APOBEC3G/APOBEC3F.
- To elucidate the distinct mechanisms by which Vif interacts with APOBEC3G and APOBEC3F.
Main Methods:
- Site-directed mutagenesis of HIV-1 Vif.
- Single-cycle infectivity assays to monitor viral growth.
- Equilibrium density centrifugation to analyze Vif-APOBEC3G/APOBEC3F association in virions.
Main Results:
- Growth-defective Vif mutants were unable to suppress APOBEC3G/APOBEC3F.
- Mutations in the C-terminal region of Vif abolished suppression of both APOBEC3G/APOBEC3F.
- Some N-terminal Vif mutants could neutralize APOBEC3G or APOBEC3F individually, indicating differential interactions.
- APOBEC3G and APOBEC3F exhibited distinct association patterns with Vif in virions.
Conclusions:
- The interaction of HIV-1 Vif with APOBEC3G is distinct from its interaction with APOBEC3F.
- Both APOBEC3G and APOBEC3F are essential targets for Vif-mediated antagonism.
- The N-terminal and C-terminal regions of Vif play differential roles in APOBEC3G/APOBEC3F antagonism.
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