Signaling through RIG-I and type I interferon receptor: Immune activation by Newcastle disease virus in man versus immune evasion by Ebola virus (Review)

In this review, two types of RNA viruses are compared with regard to the type I interferon (IFN) response in order to obtain a better understanding of the molecular mechanisms of immune activation or evasion. Upon human infection, both viruses exert either beneficial or detrimental effects. The Newcastle disease virus (NDV), is a type strain for avian paramyxoviruses, while the Ebola virus (EBOV), is a virus affecting primates. During evolution, both viruses specifically adapted to their respective hosts, acquiring sophisticated viral escape mechanisms. Two types of receptors play an important role in the life cycle of these two viruses: cytoplasmic retinoic acid-inducible gene I (RIG-I) and membrane expressed type I IFN receptor (IFNAR). In mouse and human cells, NDV is a strong inducer of the type I IFN response. The early phase of this is initiated by signaling through RIG-I and the late response by signaling through IFNAR. EBOV does not induce type I IFN responses in humans as it has viral proteins that specifically and strongly interfere with RIG-I and IFNAR signaling, as well as immune activation. In this review, we discuss whether the beneficial effects of one virus can be exploited in the fight against the detrimental effects of the other.