Alternative Splicing in Human Viral Oncogenesis and Tumor Progression

Area of Science:

• Molecular Biology
• Virology
• Oncology

Background:

• Oncogenic viruses cause 12-20% of human cancers globally.
• Tumorigenesis involves viral integration, cell cycle alteration, and immune evasion.
• Low mutation rates in oncoviral cancers suggest alternative splicing is crucial.

Purpose of the Study:

• To review oncovirus-induced alternative splicing as a driver of cancer.
• To detail how oncoviruses manipulate host splicing machinery.
• To explore therapeutic avenues targeting this mechanism.

Main Methods:

• Review of literature on human oncoviruses and alternative splicing.
• Comparison of viral hijacking strategies.
• Analysis of alternatively spliced protein isoforms in cancer hallmarks.

Main Results:

• Oncoviruses exploit host splicing for viral protein production and replication.
• Viral proteins can inhibit tumor suppressors or alter host splicing factors.
• Aberrant host transcripts and oncogenic isoforms promote cell transformation and metastasis.

Conclusions:

• Oncovirus-induced alternative splicing is a fundamental, underappreciated oncogenic mechanism.
• Understanding these pathways reveals complex interactions promoting tumor progression.
• Targeting alternative splicing offers novel therapeutic opportunities for oncoviral cancers.