Molecular arms races at the virus-host splicing interface and their pathogenic implications

Area of Science:

• Molecular Biology
• Virology
• Genomics

Background:

• RNA splicing generates transcriptomic and proteomic diversity in eukaryotes.
• Viruses like adenovirus, HIV-1, and influenza virus exploit host splicing machinery.
• This hijacking maximizes viral coding capacity and regulates infection timing.

Purpose of the Study:

• To review molecular mechanisms of viral RNA splicing.
• To illustrate how viruses co-opt host spliceosomes and reprogram splicing landscapes.
• To highlight viral circular RNAs (vcircRNAs) and their roles in immune evasion.

Main Methods:

• Review of current advances in viral RNA splicing mechanisms.
• Analysis of viral models detailing splice site selection and host-factor interactions.
• Summary of methodological breakthroughs like long-read sequencing and single-cell analyses.

Main Results:

• Viruses employ convergent strategies for alternative splice site selection.
• Viral RNA elements dynamically interact with host trans-acting factors.
• Viral circular RNAs (vcircRNAs) are generated via non-canonical back-splicing and aid immune evasion.

Conclusions:

• The virus-host splicing interface presents critical vulnerabilities.
• Understanding viral splicing offers avenues for next-generation antiviral interventions.
• This review provides an integrated perspective on viral RNA splicing and host interactions.