Skandalis et al. 



JESO Volume 139, 2008 



transmission of genetic information of both the host and the virus. In mammalian 

 systems, it appears that splicing of host genes disrupts viral infection. Herpes simplex 

 virus, vaccinia virus and adenovirus decrease splicing of cellular pre-mRNAs by inducing 

 hypo-phosphorylation of the human ASF/SF2 protein, a member of the evolutionary 

 conserved SR family of splicing factors (Kanopka et al. 1996; Huang et al. 2002; Sciabica 

 et al. 2003). Differential expression of several host splicing factors was also observed 

 following cytomegalovirus infection (Adair et al. 2004). Rous sarcoma virus (RSV) 

 contains a negative regulator of viral splicing, and is has been hypothesized that the 

 suppression of splicing benefits the virus by increasing the pool of unspliced viral RNA 

 that will be packaged as progeny genome (Maciolek and McNally 2007). 



To our knowledge this is the first report that infection may be accompanied 

 by a general splicing instability in Drosophila. Given the similarities in immune 

 responses between mammals and Drosophila, reviewed in (Muller et al. 2008) it may 

 have far reaching implications about metazoan defenses against infection. It would be 

 a great interest for infection treatment to determine in future experiments whether this 

 phenomenon constitutes an adaptive defensive strategy by the host or simply a by-product 

 of other anti-viral responses. 



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