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Related Experiment Videos

Human immunodeficiency virus type 1 escape from RNA interference.

Daniel Boden1, Oliver Pusch, Frederick Lee

  • 1Laboratory of Retrovirology, Division of Infectious Diseases, Department of Medicine, Brown Medical School, Providence, Rhode Island 02903, USA.

Journal of Virology
|October 15, 2003
PubMed
Summary

Short interfering RNA (siRNA) can inhibit human immunodeficiency virus type 1 (HIV-1) replication. However, mutations in the viral genome can lead to resistance, limiting the durability of RNA interference therapy.

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Area of Science:

  • Molecular Biology
  • Virology
  • Immunology

Background:

  • Short interfering RNA (siRNA) offers a method for sequence-specific messenger RNA (mRNA) degradation.
  • This technique can selectively inhibit viral proteins essential for human immunodeficiency virus type 1 (HIV-1) replication.

Purpose of the Study:

  • To assess the potency and durability of virus-specific RNA interference (RNAi).
  • To investigate RNAi efficacy in cell lines stably expressing short hairpin RNA (shRNA) targeting the HIV-1 transactivator protein (tat) gene.

Main Methods:

  • Stable expression of shRNA targeting the HIV-1 tat gene in cell lines.
  • Monitoring of antiviral activity and viral quasispecies evolution.

Main Results:

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  • Antiviral activity of tat shRNA was lost.
  • Emergence of HIV-1 quasispecies with point mutations in the shRNA target region caused resistance.

    • Conclusions:

    • Durable suppression of HIV-1 replication via RNAi may require targeting highly conserved viral genome regions.
    • Developing DNA constructs expressing multiple siRNAs against different viral targets could overcome resistance and reduce escape mutant probability, similar to current antiviral drug strategies.