Cells are equipped with mechanisms that allow them to rapidly detect and respond to viruses. These defense mechanisms rely partly on receptors that monitor the cytosol for the presence of atypical nucleic acids associated with virus infection. RIG-I-like receptors detect RNA molecules that are absent from the uninfected host. DNA receptors alert the cell to the abnormal presence of that nucleic acid in the cytosol. Signaling by RNA and DNA receptors results in the induction of restriction factors that prevent virus replication and establish cell-intrinsic antiviral immunity. In light of these formidable obstacles, viruses have evolved mechanisms of evasion, masking nucleic acid structures recognized by the host, sequestering themselves away from the cytosol or targeting host sensors, and signaling adaptors for deactivation or degradation. Here, we detail recent advances in the molecular understanding of cytosolic nucleic acid detection and its evasion by viruses.
"During pathogen infection, these PRRs confer the recognition of PAMPs and then trigger the downstream signaling cascade to alert the immune system to take necessary countermeasures. RLRs, a pivotal cytosolic antiviral immune PRR family, contains three members: retinoic acid-inducible gene I (RIG-I), melanoma differentiation-associated gene 5 (MDA5) and laboratory of genetics and physiology 2 (LGP2) . MDA5 and RIG-I have homologous core structural domains including two tandem caspase activation recruitment domains (CARD), a central DExD/H box RNA helicase domain and a C-terminal repressor domain (RD)  . "
"RLRs initiate signaling through IFNb-promoter stimulator-1 (IPS-1, also named Cardif, MAVS or VISA), leading to the activation of IFN regulatory factor (IRF) and nuclear factor-jB (NF-jB) pathways. Activation of the transcription factors IRF3, IRF7 and NF-jB is responsible for the transcription of genes coding for type I IFNs (IFNa and IFNb) and pro-inflammatory cytokines like IL-6 or TNFa, respectively . These processes constitute the first steps of the innate response giving rise to an anti-viral defense within infected tissues, prior the intervention of the adaptive immune system. "
" - I , MDA5 , or their variants and challenged with the viruses engineered to express a reporter gene , GFP , or with wild - type non - reporter IAV . Effi - ciency of virus spread , as measured by the number of GFP - or anti - IAV - NP - positive cells , was assessed ( Figure 4A ) . Consistent with their reported divergence in viral specificity ( Goubau et al . , 2013 ; Kato et al . , 2011 ) , full - length RIG - I and MDA5 suppressed different families of RNA viruses ( Figure 4A"
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