Journal
BIOCHEMICAL JOURNAL
Volume 445, Issue -, Pages 145-156Publisher
PORTLAND PRESS LTD
DOI: 10.1042/BJ20120413
Keywords
alternative splicing; cancer; disease therapy; tumour virus
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Funding
- CONACYT scholarship from the Mexican Government [309211]
- Wellcome Trust [088848/Z/09/Z]
- MRC-University of Glasgow Centre for Virus Research
- Wellcome Trust [088848/Z/09/Z] Funding Source: Wellcome Trust
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Persistent infection with cancer risk-related viruses leads to molecular, cellular and immune response changes in host organisms that in some cases direct cellular transformation. Alternative splicing is a conserved cellular process that increases the coding complexity of genomes at the pre-mRNA processing stage. Human and other animal tumour viruses use alternative splicing as a process to maximize their transcriptomes and proteomes. Medical therapeutics to clear persistent viral infections are still limited. However, specific lessons learned in some viruses [e.g. HIV and HCV (hepatitis C virus)] suggest that drug-directed inhibition of alternative splicing could be useful for this pug:lose. The present review describes the basic mechanisms of constitutive and alternative splicing in a cellular context and known splicing patterns and the mechanisms by which these might be achieved for the major human infective tumour viruses. The roles of splicing-related proteins expressed by these viruses in cellular and viral gene regulation are explored. Moreover, we discuss some currently available drugs targeting SR (serine/arginine-rich) proteins that are the main regulators of constitutive and alternative splicing, and their potential use in treatment for so-called persistent viral infections.
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