Sendai virus C proteins must interact directly with cellular components tointerfere with interferon action

Sendai virus (SeV) infection of interferon (IFN)-competent cells is one of the most efficient ways of inducing IFN production. Virus replication is ne vertheless largely unaffected, since SeV infection also interfers with IFN action, a prerequisite for the establishment of an antiviral state. This pr operty has been mapped by reverse genetics to the viral C gene, which is al so known to act as a promoter-specific inhibitor of viral RNA synthesis. Us ing luciferase reporter plasmids containing IFN-responsive promoters, we ha ve found that all four C proteins effectively interdict IFN signaling when expressed independently of SeV infection. The C proteins must therefore int eract directly with cellular components to carry this out. The C gene in th e context of an SeV infection was also found to induce STAT1 instability in some cells, whereas in other cells it apparently acts to prevent the synth esis of STAT1 in response to the virus infection or IFN treatment. The SeV C proteins appear to act in at least two ways to counteract the IFN induced by SeV infection.