Sendai Virus (SeV) is an enveloped virus of 150–250 nm in diameter whose genome is a single chain RNA in the minus sense. Six genes coding for viral proteins are situated sequentially on the genome of the wild-type SeV in the following order.
Nucelocapsid protein (NP) forms the core nucleocapsid complex with the genome RNA. Phosphoprotein (P) is the small subunit of the RNA polymerase. Matrix protein (M) supports the envelope structure from the inside. Fusion protein (F) fuses the viral envelope with the cell membrane when the virus enters the cell. The gene encoding the F protein is deleted from the CytoTune® -iPS Sendai Reprogramming Kit vectors, rendering them incapable of producing infectious particles from infected cells.
Hemagglutinin-Neuraminidase (HN) recognizes the cell surface receptor, sialic acid. Large protein (L) is the large subunit of RNA polymerase.
Because SeV infects cells by attaching itself to the sialic acid receptor present on the surface of many different cells, it can infect a wide range of cell types of various animal species. Activation of F protein by a protease is required for the virus-cell fusion process to take place. After infection, the virus goes through genome replication and protein synthesis in the cytoplasm, and then daughter virus particles are assembled and released.
Other viral vectors, such as lentivirus or retrovirus, require integration into the host genome for replication and can therefore disrupt the genome of the cells that are reprogrammed rendering iPSCs and their derivatives less safe for clinical applications or altering gene expression patterns which can compromise compound screens or disease pathway analyses. A single transduction with the CytoTune® -iPS Sendai Reprogramming Kit generates iPSCs at high efficiency with no genomic integration or viral remnants allowing the use of iPSCs and their derivatives in a broader range of research experiments.