Viruses are a class of highly diverse pathogens which depend on the host cell for their replication. The initiation of a protective innate antiviral immune response involves the action of specialized pattern recognition receptors (PRR), which detect conserved molecular structures of the invading pathogen. Triggering of PRRs induces the production of host proinflammatory cytokines (e.g. TNF, IL-6 and IL-1) and type I interferons (interferon-α (IFN-α) and IFN-β) through activation of downstream signaling pathways that control various transcription factors such as NF-κB, AP-1, IRF3 and IRF7 [1], [2]. The presence of viral nucleic acids, such as viral RNA and DNA, viral replication intermediates and viral transcription products, can be sensed by specific intracellular PRRs [3]. Endosomal Toll-like receptors (TLRs) and cytoplasmic RNA helicase RIG-I-like receptors (RLRs) or Nod-like receptors (NLRs) detect the presence of viral single stranded (TLR7, TLR8, Nod2) or double stranded RNA (TLR3, RIG-I, MDA5). Intracellular DNA sensors that mediate antiviral immune responses to DNA viruses include TLR9, DAI [4] and the PYHIN domain containing proteins AIM2 [5], [6], [7] and IFI16 [8]. TLR mediated antiviral responses are restricted to specialized type I IFN producing plasmacytoid dendritic cells (pDC), while most other cell types, including conventional DC (cDC), macrophages and fibroblasts, depend on the cytosolic RNA and DNA sensors for the production of antiviral proteins [9].