This formation involves the fusion of infected cells with adjacent target cells and remains an important mechanism of direct cell-to-cell spread of viral components. Thus, a SeV infection in a form of genetic material in partially assembled virions can spread without any exposure to host neutralizing antibodies (see the section "Directed cells fusion (syncytium formation) for details and references). Sendai virus, as all other envelope viruses, uses host cellular membrane lipid bilayer for viral capsid membrane formation. Binding to a host cell membrane of viral proteins (M, HN and F) promotes their interaction with RNP complex, which is composed of the viral genomic RNA bound to SeV proteins (NP, P and L). Thus, all viral structural components, including viral glycoproteins and genomic RNP complex, are getting assembled together. After such assembling the infectious viral particles are budding out from individually or collectively infected cells (syncitia). C-protein facilitates budding by interacting with AIP1/Alix, which is a host protein that is involved in apoptosis and endosomal membrane trafficking. The infectious virus particles usually released by 24 hours post infection (hpi), and peak titers appeared between 48 and 72 hpi. Sendai virus can establish persistent infection in its host cells. Multiple rounds of virus sub-culturing result in a creation of new virus variants with high ability to establish persistent infection. These SeV variants develop certain genotypic changes. The persistent infection can also be established instantly in interferon regulatory factor 3 (IRF-3)-knockdown cells. IRF-3 is a key proapoptotic protein that after activation by SeV triggers apoptosis. IRF-3-knockdown cells express viral protein and produces low levels of infectious virions. IRF-3 controls the fate of the SeV-infected cells by triggering apoptosis and preventing persistence establishment; therefore its knock down allows persistence to occur. It was also reported that during SeV infection replication defective viral genomes (DVG) are forming and selectively protect a sub-population of host cells from death, therefore promoting the establishment of persistent infections. In nature enzootic disease patterns suggest that the virus can be latent and can be cleared over the course of a year. One recognized feature of the Sendai virus, shared with members of its genus, is the ability to induce syncytia formation "in vivo" and "in vitro" in eukaryotic cell cultures. The formation of syncytium helps the virus to avoid neutralizing antibodies of the host organism during the spread of infection.The mechanism for this process is fairly well understood and is very similar to the fusion process employed by the virion to facilitate cellular entry.