ABSTRACT
The human body and in particular the human immune system have evolved a large number of mechanisms to control viral infections. Multiple mechanical and immunological barriers exist that inhibit and restrict viral entry, infections as well as replication. A rst barrier is the surface of the body, which usually does not allow penetration by viral particles and blocks viral infection from the very start. If viruses successfully overcome this rst barrier, a number of innate sensing mechanisms exist in practically every cell type (e.g., RIG-I, Mda5, LGP2, STING, AIM2 [Imaizumi et al. 2002; Gitlin et al. 2006; Ishikawa et al. 2009; Schmidt et al. 2009; Satoh et al. 2010; Barber 2011]). These intracellular molecules sense viral infection, causing the production of type I IFN, which globally inhibits viral replication by inducing degradation of viral nucleic acids or inhibition of viral replication (Bowie and Unterholzner 2008; Yan and Chen 2012). Plasmacytoid dendritic cells (pDCs) of the innate immune system have evolved a particularly powerful sensing system for viral infection and are the dominant producers of antiviral type I interferon (Colonna et al. 2004; McKenna et al. 2005). In addition to recognition of viral nucleic acids, both the innate and adaptive immune systems have evolved various ways to recognize and inactivate exogenous viral particles as well as infected cells (Zinkernagel 1996). Both arms of the immune system collaborate to achieve maximal specic immune responses.
