Key result
A chimeric, replication-deficient influenza A virus vector was developed by fine-tuning NS2/NEP mRNA splicing efficacy to achieve genetic stability and high transgene expression levels.
A novel chimeric, replication-deficient influenza A virus vector was established by modulating splicing efficiency to stably express high levels of transgenes.
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Supports stable cytokine-expressing influenza vectors via splicing optimization; leaves open therapeutic applications pending validation.
Segment 8 of the influenza A virus codes for two proteins (NS1 and NS2/NEP) via splicing. Here, we developed a viral vector expressing a cytokine or chemokine instead of the interferon antagonist NS1. To achieve both the desired genetic stability and high transgene expression levels, NS2/NEP mRNA splicing efficacy had to be fine-tuned by modification of splicing elements. Expression levels of secreted foreign proteins could be further enhanced by fusing the N-terminal 13 amino acids of NS1 with an IgK-derived secretion signal peptide. Thus, the first start codon was used for translation initiation of both NS2/NEP and the foreign protein.
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Wolschek et al. (2010) studied this question. Chimeric, replication-deficient influenza A virus vector was evaluated on Genetic stability and transgene expression levels. A chimeric, replication-deficient influenza A virus vector was developed by fine-tuning NS2/NEP mRNA splicing efficacy to achieve genetic stability and high transgene expression levels.
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