Utilizing the codon adaptation index to evaluate the susceptibility to HIV-1 and SARS-CoV-2 related coronaviruses in

Haoyu Zhou1,2, Ruohan Ren1,3, Stephen Shing-Toung Yau1,4

  • 1Yanqi Lake Beijing Institute of Mathematical Sciences and Applications (BIMSA), Beijing, China.

Insights

This study used the codon adaptation index (CAI) to assess human cell susceptibility to HIV-1 and SARS-CoV-2. Viral CAI values were generally lower than endogenous genes, suggesting incomplete adaptation, but CAI can aid in predicting viral target cells.

Area of Science:

  • Virology
  • Molecular Biology
  • Bioinformatics

Background:

  • Viral susceptibility is determined by factors including cell surface receptors and efficient viral gene expression.
  • Translational efficiency, influenced by codon adaptation, is critical for viral gene expression and infection.
  • Codon Adaptation Index (CAI) measures translational efficiency at the elongation level.

Purpose of the Study:

  • To evaluate human cell susceptibility to HIV-1 and SARS-CoV-2 using CAI.
  • To refine viral infectivity analysis to the cell-type level.
  • To investigate the impact of viral infection on cellular translational mechanisms.

Main Methods:

  • Calculated CAI for viral open reading frames (ORFs) in various human cell types.
  • Correlated CAI with translational efficiency using endogenous genes as a benchmark.
  • Compared CAI-based susceptibility predictions with experimental findings.

Main Results:

  • Viral ORFs generally exhibited lower CAI values compared to highly expressed endogenous genes, indicating suboptimal adaptation to host translational machinery.
  • CAI-based susceptibility predictions largely aligned with experimental data, though exceptions were noted.
  • HIV-1 infection decoupled CAI and translational efficiency of endogenous genes, while SARS-CoV-2 increased viral ORF CAI in infected cells.

Conclusions:

  • CAI serves as a valuable auxiliary index for assessing cell susceptibility to viruses like HIV-1 and SARS-CoV-2.
  • CAI alone is insufficient for definitively identifying viral target cells.
  • Different viruses modulate host cellular translational mechanisms distinctively.

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