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Updated: Jun 25, 2026

Evaluation of the Efficacy And Toxicity of RNAs Targeting HIV-1 Production for Use in Gene or Drug Therapy
Published on: September 5, 2016
Inhibition of HIV-1 replication by eIF3f
Susana T Valente1, Greg M Gilmartin, Christina Mott
1Department of Biochemistry and Molecular Biophysics, Howard Hughes Medical Institute, College of Physicians and Surgeons, Columbia University, HHSC 1310c, 701 West 168th Street, New York, NY 10032, USA. sv2033@columbia.edu
Eukaryotic initiation factor 3 subunit f (eIF3f) inhibits HIV-1 replication. Overexpression of eIF3f or its fragment N91-eIF3f restricts viral mRNA levels by interfering with HIV-1 mRNA 3' end processing.
Area of Science:
- Virology
- Molecular Biology
- Gene Expression
Background:
- Viruses rely on host cell machinery for replication.
- Identifying host factors is crucial for understanding viral replication and developing antivirals.
Purpose of the Study:
- To identify host factors that interfere with Human Immunodeficiency Virus type 1 (HIV-1) replication.
- To investigate the mechanism by which the identified host factor restricts viral replication.
Main Methods:
- Screening of cDNA expression libraries to find inhibitors of HIV-1 vector transduction.
- Overexpression of candidate host factors (N91-eIF3f and full-length eIF3f).
- Quantification of viral mRNA levels and analysis of 3' end processing of viral mRNA.
Main Results:
- The N-terminal 91 amino acids of eukaryotic initiation factor 3 subunit f (N91-eIF3f) potently inhibited HIV-1 expression.
- Overexpression of N91-eIF3f or full-length eIF3f significantly reduced nuclear and cytoplasmic viral mRNA levels.
- eIF3f and N91-eIF3f were shown to specifically target the 3' long terminal repeat (3'LTR) region of HIV-1 mRNA.
- The 3' end cleavage of HIV-1 mRNA precursors was specifically reduced in cells expressing N91-eIF3f.
Conclusions:
- Eukaryotic initiation factor 3 subunit f (eIF3f) plays a role in mRNA maturation.
- eIF3f can specifically interfere with the 3' end processing of HIV-1 mRNAs, thereby restricting viral replication.
- These findings suggest eIF3f as a potential target for antiviral strategies against HIV-1.
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