In a separate perspective, virus infection can trigger through double-stranded viral RNAs an innate antiviral immune response. Thus viral dsRNAs can be recognized by cellular proteins [pattern-recognition receptors (PRRs)] which initiate antiviral responses by inducing the production of a variety of cytokines including type I interferons (IFN-a and IFN-b) and initiating additional inflammatory and adaptive immune responses. Recently, DExD/H RNA helicases such as RIG-1 (retinoic acid inducible gene-1) (93) and Mda5 (melanoma differentiation-associated gene 5) (94) have been identified as suppressors of viral replication by binding to virus associated dsRNA and activating type I interferon-dependent antiviral immunity. Over-expression of RIG-1 and Mda5 was found to enhance dsRNA induced type I interferon antiviral response. Currently, it remains speculative whether helicases like RIG-1 and Mda5 may recognize HIV-1 dsRNA and trigger an innate immune response. Intriguingly, several reports exist in the literature that HIV-1 infection does induce activation of type 1 interferons (95, 96) .