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Updated: Oct 8, 2025

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
Crosstalk between R848 and abortive HIV-1 RNA-induced signaling enhances antiviral immunity
Melissa Stunnenberg1, John L van Hamme1, Esther M Zijlstra-Willems1
1Department of Experimental Immunology, Amsterdam institute for Infection & Immunity, Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands.
Abstract:
Pathogens trigger multiple pattern recognition receptors (PRRs) that together dictate innate and adaptive immune responses. Understanding the crosstalk between PRRs is important to enhance vaccine efficacy. Abortive HIV-1 RNA transcripts are produced during acute and chronic HIV-1 infection and are known ligands for different PRRs, leading to antiviral and proinflammatory responses. Here, we have investigated the crosstalk between responses induced by these 58 nucleotide-long HIV-1 RNA transcripts and different TLR ligands. Costimulation of dendritic cells (DCs) with abortive HIV-1 RNA and TLR7/8 agonist R848, but not other TLR agonists, resulted in enhanced antiviral type I IFN responses as well as adaptive immune responses via the induction of DC-mediated T helper 1 (TH 1) responses and IFNγ+ CD8+ T cells. Our data underscore the importance of crosstalk between abortive HIV-1 RNA and R848-induced signaling for the induction of effective antiviral immunity.
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