Innate immune response against nonsegmented negative strand RNA viruses.
Innate immune response represents the hallmark of host defense against foreign pathogens, including viruses. Not only does this response combat viruses during initial stages of infection, but it shapes the adaptive immune response as well. This review focuses on this critical host defense mechanism, the innate immune response, in the context of infection by nonsegmented negative strand RNA viruses of the Paramyxoviridae family. We specifically focus on the two critical transcription factors, nuclear factor-kappaB (NF-kappaB) and interferon (IFN) regulatory factor-3 (IRF-3), that play an important role in establishing an innate antiviral state. The antiviral cytokine IFN-alpha/beta (IFN type I) produced following viral infection as a result of activation of NF-kappaB or IRF-3 or both exerts an antiviral state by inducing the Janus kinases/signal transducer and activator (Jak-Stat) pathway. In that context, our review discusses various strategies adopted by these viruses to counteract and evade the antiviral action of IFN I for replicative advantages, especially after modulation of the Jak-Stat antiviral pathway. Understanding this interplay between the innate immune response and viral replication is fundamental to probing into the molecular basis of host-virus interaction.
D004268:DNA-Binding Proteins / Q000502:physiology; D006801:Humans; D007113:Immunity, Innate; D050838:Interferon Regulatory Factor-3; D007370:Interferon Type I / Q000502:physiology; D016328:NF-kappa B / Q000502:physiology; D010252:Paramyxoviridae / Q000235:genetics / Q000472:pathogenicity / Q000502:physiology; D018184:Paramyxoviridae Infections / Q000276:immunology* / Q000821:virology; D015398:Signal Transduction; D014157:Transcription Factors / Q000502:physiology; D014779:Virus Replication
D004268:DNA-Binding Proteins; C494232:IRF3 protein, human; D050838:Interferon Regulatory Factor-3; D007370:Interferon Type I; D016328:NF-kappa B; D014157:Transcription Factors