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A growing body of evidence has demonstrated the role of components of innate immunity, including Toll-like receptors (TLRs), the retinoic acid-inducible gene I/melanoma-differentiation factor 5 (RIG-I/MDA5) and microRNAs (miRNAs) in the recognition of dengue virus (DENV) or its components by infected cells. TLR3, TLR7/8 and RIG-I/MDA5 sense genomic RNA or dsRNA, the product of an intermediate step of DENV replication, activating intracellular pathways leading to the production of antiviral effectors, including interferon and pro-inflammatory cytokines. Recognition by TLR2 and TLR4 also promotes the activation of other intracellular pathways and alters viral replication in an interferon-independent manner. It was also recently demonstrated that cellular miRNAs, a class of post-transcriptional regulatory small RNAs, can affect replication. To accomplish this, miRNAs bind either directly to viral RNA, through base-pair complementarity affecting translation, or indirectly through virus-mediated changes in host protein expression in the viral life cycle. There is also evidence that certain miRNAs can recognize or be recognized by TLRs and RIG-I/MDA5, resulting in alteration of the innate immune response. In this review, we summarize our present knowledge of DENV-host factor interactions, emphasizing the role of TLRs, RIG-I/MDA5 and miRNAs and their possible connection with pathogenesis. Our discussion is based on recent reports suggesting how these different innate immune components might be activated to induce an antiviral response, and how DENV has developed mechanisms to manipulate or evade these antiviral activities.Interaction between dengue virus and pathogen recognition receptors alters the production of pro-inflammatory cytokines.Cellular miRNA could either promote or decrease DENV replication.Viral components such as proteins and sfRNA block the expression of RIG-I/MDA5.The interaction of NS3 with hHSP70 perturbs RNA-induced silencing complex formation, impairing miRNA activity.Intracellular PRRs recognize viral RNAs and induce the expression of type I interferon and interferon-stimulated genes.