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Updated: May 13, 2025

Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells
Published on: April 26, 2017
The Emerging Roles of Alternative Splicing in Human Oncovirus Infection
Xuefei Liao1, Li Yang1, Mingjuan Jiang1
1Department of Microbiology, Xiangya School of Basic Medical Sciences, Central South University, Changsha, Hunan, China.
Abstract:
Alternative splicing (AS) is one of the most potent mechanisms for expanding the diversity of proteomes. During infection, human oncogenic viruses may exploit the AS to facilitate their replication cycle. Moreover, persistently infecting viruses can target key genes involved in classical signaling pathways to promote viral persistence and tumor progression. Here, we highlight how oncogenic viruses hijack AS system to manipulate host biological processes, and the host's AS system in turn modulates viral infection and replication. In addition, we have summarized the relatively underexplored involvement of noncoding RNAs in AS following tumor virus infection. This bidirectional interaction provides novel insights into interaction of virus-host and opens new avenues for therapeutic strategies targeting oncogenic viral infections.
Insights
Oncogenic viruses manipulate alternative splicing (AS) to aid replication and promote tumors. Understanding this virus-host interaction, including noncoding RNAs, offers new therapeutic targets for viral infections.
Area of Science:
- Molecular Biology
- Virology
- Genetics
Background:
- Alternative splicing (AS) significantly expands proteome diversity.
- Oncogenic viruses can exploit host AS machinery for replication and to promote viral persistence and tumor development.
- Viruses can target host signaling pathways, influencing viral infection and disease progression.
Purpose of the Study:
- To review how oncogenic viruses utilize the host's AS system.
- To explore the reciprocal modulation of viral infection by the host's AS system.
- To summarize the role of noncoding RNAs in AS during tumor virus infections.
Main Methods:
- Literature review and synthesis of current research on virus-host interactions.
- Analysis of molecular mechanisms underlying alternative splicing manipulation by oncogenic viruses.
- Investigation into the role of noncoding RNAs in alternative splicing during viral infections.
Main Results:
- Oncogenic viruses hijack host AS to manipulate cellular processes and facilitate their life cycle.
- Host AS machinery can influence viral replication and infection outcomes.
- Noncoding RNAs play an underappreciated role in AS following oncogenic virus infection.
Conclusions:
- The bidirectional interplay between oncogenic viruses and host AS provides critical insights into virus-host interactions.
- Targeting virus-hijacked AS pathways presents novel therapeutic opportunities for oncogenic viral infections.
- Further research into noncoding RNA involvement in AS during viral infections is warranted.
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