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Updated: Aug 2, 2026
18:10
Isolation of Fidelity Variants of RNA Viruses and Characterization of Virus Mutation Frequency
Published on: June 16, 2011
[Sequence variation of HIV and bioinformatics].
1Integrated Database Team, Biological Information Research Center, National Institute of Advanced Industrial Science and Technology, 2-41-6 Aomi, Koto-ku, Tokyo 135-0064, Japan. yyamaguc@jbirc.aist.go.jp
Uirusu
|September 29, 2004
Summary
Human immunodeficiency virus type 1 (HIV-1) envelope glycoprotein evolution reveals sites under positive selection for immune evasion. Specific amino acid variations, like at residue 440, influence the virus
Area of Science:
- Virology
- Evolutionary Biology
- Immunology
Context:
- The human immunodeficiency virus type 1 (HIV-1) envelope glycoprotein (gp120) is crucial for viral entry into host cells.
- gp120 interacts with cellular receptors and mediates membrane fusion, a process essential for viral infectivity.
- Amino acid variability in gp120 is driven by evolutionary pressures, including host immune system evasion and receptor binding.
Purpose:
- To elucidate the evolutionary mechanisms of the HIV-1 gp120 envelope glycoprotein at the single amino acid site level.
- To identify specific amino acid positions under positive and negative selection.
- To determine amino acid positions responsible for the usage of the co-receptor CXCR4.
Summary:
- Analysis of 186 HIV-1 gp120 (subtype B) sequences identified 33 amino acid positions potentially under positive selection, suggesting roles in immune evasion and epitope formation.
- The study reevaluated amino acid variability and estimated synonymous and nonsynonymous substitutions to detect selection pressures.
- Beyond the V3 loop, amino acid variation at residue 440 in the C4 region was found to be significantly linked with CXCR4 co-receptor usage.
Impact:
- Provides a detailed understanding of the evolutionary dynamics of HIV-1 gp120, crucial for vaccine development and antiviral strategies.
- Identifies key residues involved in viral entry and host immune system interaction, potentially revealing new targets for therapeutic intervention.
- Highlights the complex interplay between viral evolution, receptor binding, and immune escape mechanisms in HIV-1 pathogenesis.
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