The oncogenic gamma herpesviruses Epstein-Barr virus (EBV) and Kaposi’s  sarcoma-associated herpesvirus (KSHV) hijack retinoic acid-inducible gene  I (RIG-I) facilitating both viral and tumour immune evasion

Herpesviruses evade host immunity to establish persistent lifelong infection with dormant latent and replicative  lytic phases. Epstein-Barr virus (EBV) and Kaposi’s Sarcoma-associated virus (KSHV) are double-stranded DNA  herpesviruses that encode components to activate RNA sensors, (Retinoic acid-inducible gene I (RIG-I) and  melanoma differentiation-associated protein 5 (MDA5). Yet both viruses can effectively evade the antiviral  immune response. The ability of these viruses to disarm RIG-I to evade immunity allowing viral persistency can  contribute to the creation of a protected niche that facilitates tumour growth and immune evasion. Alternatively,  viral nucleic acids present in the cytosol during the replicative phase of the viral lifecycle can activate proinflammatory signaling downstream of RIG-I augmenting tumour promoting inflammation.  Understanding how these viral proteins disrupt innate immune pathways could help identify mechanisms to  boost immunity, clearing viral infection and enhancing the efficacy of immunotherapy for virally induced  cancers. Here we review literature on the strategies EBV and KSHV use to either enhance or inhibit RLR  signaling.