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Evaluation of the Efficacy And Toxicity of RNAs Targeting HIV-1 Production for Use in Gene or Drug Therapy
Published on: September 5, 2016
HIV-1 modulates the tRNA pool to improve translation efficiency
Anna van Weringh1, Manon Ragonnet-Cronin, Erinija Pranckeviciene
1Department of Biology, University of Ottawa, Ottawa, Ontario, Canada.
Molecular Biology and Evolution
|January 11, 2011
Summary
Human immunodeficiency virus type 1 (HIV-1) efficiently expresses genes despite poor codon usage by packaging specific transfer RNAs (tRNAs). These enriched tRNAs, particularly those for A-ending codons, suggest host tRNA alterations during infection.
Area of Science:
- Virology
- Molecular Biology
- Genetics
Background:
- Human immunodeficiency virus type 1 (HIV-1) exhibits efficient replication and expression in human cells despite suboptimal codon usage.
- HIV-1 packages non-lysyl transfer RNAs (tRNAs) alongside the essential tRNA(Lys) for viral replication processes.
Purpose of the Study:
- To investigate the relationship between HIV-1 codon usage and the tRNA pool within host cells.
- To determine if HIV-1 selectively packages specific tRNAs and if this packaging is linked to viral gene expression.
Main Methods:
- Comparative analysis of HIV-1 gene codon usage against human host codon usage.
- Examination of tRNA composition within HIV-1 virions.
Main Results:
- HIV-1 virions are enriched in tRNAs that decode codons highly favored by HIV-1 but rarely used by the human host.
- A significant enrichment of tRNAs decoding A-ending codons was observed, correlating with HIV-1's A-rich genome.
- HIV-1 late genes show better adaptation to the selectively enriched tRNA pool, suggesting dynamic changes during infection.
Conclusions:
- HIV-1 packaging of tRNAs appears to be a passive process reflecting the host cell's tRNA availability during virion formation.
- The selective enrichment of specific tRNAs suggests that HIV-1 may induce alterations in the host tRNA pool late in infection.
- HIV-1 exhibits a degree of codon adaptation to the host's tRNA environment, potentially exceeding previous estimations.
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