Targeting Type I Interferon Induction and Signaling: How Zika Virus Escapes from Host Innate Immunity

• Published in: International journal of biological sciences Vol. 19; no. 10; pp. 3015 - 3028
• Main Authors: Hu, Huan, Feng, Yaxiu, He, Ming-Liang
• Format: Journal Article
• Language: English
• Published: Australia Ivyspring International Publisher Pty Ltd 01.01.2023; Ivyspring International Publisher
• Subjects: Antibodies; Antigens; Antiviral activity; Antiviral Agents; Cytokines; Dendritic cells; Dengue fever; Drug development; Genomes; Guillain-Barre syndrome; Humans; Immune response; Immune system; Immunity, Innate; Infections; Inflammasomes; Innate immunity; Interferon; Interferon Type I; Interferons; Kinases; Life cycles; Microcephaly; Neurological diseases; Pathogenesis; Pathogens; Phosphorylation; Proteins; Review; RNA polymerase; Signal Transduction; Structural proteins; TLR3 protein; TLR7 protein; Toll-like receptors; Vector-borne diseases; Viral infections; Virus Replication; Viruses; West Nile virus; Zika virus; Zika Virus - metabolism; Zika Virus Infection; Zika virus; interferons-stimulated genes; type I interferons
• ISSN: 1449-2288; 1449-2288
• DOI: 10.7150/ijbs.83056

Zika virus (ZIKV) infection causes neurological disorders and draws great attention. ZIKV infection can elicit a wide range of immune response. Type I interferons (IFNs) as well as its signaling cascade play crucial role in innate immunity against ZIKV infection and in turn ZIKV can antagonize them. ZIKV genome are mainly recognized by Toll-like receptors 3 (TLR3), TLR7/8 and RIG-I-like receptor 1 (RIG-1), which induces the expression of Type I IFNs and interferon-stimulated genes (ISGs). ISGs exert antiviral activity at different stages of the ZIKV life cycle. On the other hand, ZIKV takes multiple strategies to antagonize the Type Ⅰ IFN induction and its signaling pathway to establish a pathogenic infection, especially by using the viral nonstructural (NS) proteins. Most of the NS proteins can directly interact with the factors in the pathways to escape the innate immunity. In addition, structural proteins also participate in the innate immune evasion and activation of antibody-binding of blood dendritic cell antigen 2 (BDCA2) or inflammasome also be used to enhance ZIKV replication. In this review, we summarize the recent findings about the interaction between ZIKV infection and type I IFNs pathways and suggest potential strategies for antiviral drug development.