The zigzag model (Jones and Dangl, 2006) presents a classic view of the interactions between plants and non-viral pathogens. Ding (2010) considered dsRNA as the Pathogen-associated Molecular Patterns (PAMPs) of viral pathogen and RNA silencing (or RNAi) as a form of PTI against viruses. Recently, Mandadi and Scholthof (2013) further integrated these concepts into current plant-virus interaction models. In this model, dsRNAs produced during virus infection are regarded as viral PAMP; RNAi-mediated antiviral defense is analogous to PAMP-triggered immunity (PTI); viral suppressors of RNAi (VSR) such as coat proteins (CPs), movement proteins (MPs), and replicase are regarded as avirulent (Avr) factors or effectors; R gene-mediated viral resistance is considered as viral effector-triggered immunity (ETI). Moon and Park and Gouveia et al. review how this model is shaped in details. In addition, Gouveia et al. reviewed the recent progresses in antiviral immune receptors and co-receptors involved in antiviral innate immunity in plants and describe the NIK1-mediated antiviral signaling, which is specific to plant DNA viruses and relies on transmembrane receptor-mediated translational suppression for defense. It remains to be seen whether this is an exception or a common viral defense mechanism used by plants.