Innate Immune Response to Dengue Virus: Toll-like Receptors and Antiviral Response

Fernandes-Santos, Caroline; Azeredo, Elzinandes Leal de

doi:10.3390/v14050992

Cited by 31 publications

(17 citation statements)

References 134 publications

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“…In ChiLCV-infected B. tabaci, TLR3 and TOB1 were highly abundant in adult B. tabaci which might facilitate the invasion and multiplication of the virus in B. tabaci ( Nekkanti et al., 2022 ). Toll-like receptors are actively involved in innate immune responses against viruses ( Perales-Linares and Navas-Martín, 2013 ; Lester and Li, 2014 ; He et al., 2021 ) and TLR3 is involved in protective antiviral responses ( Ozato et al., 2002 ; Fernandes-Santos and Azeredo, 2022 ). Perales-Linares and Navas-Martín (2013) reported that TLR3 participates in both defense and offense in host immunity to viruses.…”

Section: Discussionmentioning

confidence: 99%

Effect of silencing Bemisia tabaci TLR3 and TOB1 on fitness and begomovirus transmission

et al. 2023

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Bemisia tabaci (Hemiptera: Aleyrodidae) is one of the most important invasive pests worldwide. It infests several vegetables, legumes, fiber, and ornamental crops. Besides causing direct damage by sucking plant sap, B. tabaci is the principal vector of begomoviruses. Chilli leaf curl virus (ChiLCV, Begomovirus) transmitted by B. tabaci is a major constraint in chilli production. B. tabaci genes associated with metabolism, signaling pathways, cellular processes, and organismal systems are highly enriched in response to ChiLCV infection. The previous transcriptome study suggested the association of B. tabaci Toll-like receptor 3 (TLR3) and transducer of erbB2.1 (TOB1) in ChiLCV infection. In the present study, B. tabaci TLR3 and TOB1 were silenced using double-stranded RNA (dsRNA) and the effect on fitness and begomovirus transmission has been reported. Oral delivery of dsRNA at 3 µg/mL reduced the expression of B. tabaci TLR3 and TOB1 by 6.77 and 3.01-fold, respectively. Silencing of TLR3 and TOB1 induced significant mortality in B. tabaci adults compared to untreated control. The ChiLCV copies in B. tabaci significantly reduced post-exposure to TLR3 and TOB1 dsRNAs. The ability of B. tabaci to transmit ChiLCV also declined post-silencing TLR3 and TOB1. This is the first-ever report of silencing B. tabaci TLR3 and TOB1 to induce mortality and impair virus transmission ability in B. tabaci. B. tabaci TLR3 and TOB1 would be novel genetic targets to manage B. tabaci and restrict the spread of begomovirus.

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Section: Discussionmentioning

confidence: 99%

Effect of silencing Bemisia tabaci TLR3 and TOB1 on fitness and begomovirus transmission

et al. 2023

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“…The innate antiviral response to DENV is initiated by various immune cells and inflammatory mediators. Macrophages and monocytes are the main targets of DENV infection, whose functions include recognizing pathogen-associated molecular patterns (PAMPs) through pattern recognition receptors (PRRs) 53 . Toll-like receptors (TLRs) are the major PRRs that are coupled to detect specific viral components and induce the production of inflammatory cytokines, chemokines, and IFNs 54 .…”

Section: Discussionmentioning

confidence: 99%

Aedes albopictus salivary adenosine deaminase is an immunomodulatory factor facilitating dengue virus replication

Mu,

Lin,

Sun

et al. 2023

Sci Rep

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The Asian tiger mosquito, Aedes albopictus, is an important vector for the transmission of arboviruses such as dengue virus (DENV). Adenosine deaminase (ADA) is a well-characterized metabolic enzyme involved in facilitating blood feeding and (or) arbovirus transmission in some hematophagous insect species. We previously reported the immunologic function of ADA by investigating its effect on mast cell activation and the interaction with mast cell tryptase and chymase. The 2-D gel electrophoresis and mass spectrometry analysis in the current study revealed that ADA is present and upregulated following mosquito blood feeding, as confirmed by qRT-PCR and western blot. In addition, the recombinant ADA efficiently converted adenosine to inosine. Challenging the Raw264.7 and THP-1 cells with recombinant ADA resulted in the upregulation of IL-1β, IL-6, TNF-α, CCL2, IFN-β, and ISG15. The current study further identified recombinant ADA as a positive regulator in NF-κB signaling targeting TAK1. It was also found that recombinant Ae. albopictus ADA facilitates the replication of DENV-2. Compared with cells infected by DENV-2 alone, the co-incubation of recombinant ADA with DENV-2 substantially increased IL-1β, IL-6, TNF-α, and CCL2 gene transcripts in Raw264.7 and THP-1 cells. However, the expression of IFN-β and ISG15 were markedly downregulated in Raw264.7 cells but upregulated in THP-1 cells. These findings suggest that the immunomodulatory protein, Ae. albopictus ADA is involved in mosquito blood feeding and may modulate DENV transmission via macrophage or monocyte-driven immune response.

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“…During virus infection, virus RNA is sensed by PRRs, which include RIG-I-like receptors (RLRs), NOD-like receptors (NLRs), and Toll-like receptors (TLRs) [34][35][36][37]. After influenza virus infection, influenza viral RNA is recognized by the RIG-I receptor, which activates and recruits the downstream TBK1/IKKγ/IKKε complex to induce IRF3 signaling, resulting in the production of type I interferons [38,39].…”

Section: Discussionmentioning

confidence: 99%

Tripartite motif-containing protein 46 accelerates influenza A H7N9 virus infection by promoting K48-linked ubiquitination of TBK1

Lin

Zhao

et al. 2022

Virol J

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Background Avian influenza A H7N9 emerged in 2013, threatening public health and causing acute respiratory distress syndrome, and even death, in the human population. However, the underlying mechanism by which H7N9 virus causes human infection remains elusive. Methods Herein, we infected A549 cells with H7N9 virus for different times and assessed tripartite motif-containing protein 46 (TRIM46) expression. To determine the role of TRIM46 in H7N9 infection, we applied lentivirus-based TRIM46 short hairpin RNA sequences and overexpression plasmids to explore virus replication, and changes in type I interferons and interferon regulatory factor 3 (IRF3) phosphorylation levels in response to silencing and overexpression of TRIM46. Finally, we used Co-immunoprecipitation and ubiquitination assays to examine the mechanism by which TRIM46 mediated the activity of TANK-binding kinase 1 (TBK1). Results Type I interferons play an important role in defending virus infection. Here, we found that TRIM46 levels were significantly increased during H7N9 virus infection. Furthermore, TRIM46 knockdown inhibited H7N9 virus replication compared to that in the control group, while the production of type I interferons increased. Meanwhile, overexpression of TRIM46 promoted H7N9 virus replication and decrease the production of type I interferons. In addition, the level of phosphorylated IRF3, an important interferon regulatory factor, was increased in TRIM46-silenced cells, but decreased in TRIM46 overexpressing cells. Mechanistically, we observed that TRIM46 could interact with TBK1 to induce its K48-linked ubiquitination, which promoted H7N9 virus infection. Conclusion Our results suggest that TRIM46 negatively regulates the human innate immune response against H7N9 virus infection.

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Innate Immune Response to Dengue Virus: Toll-like Receptors and Antiviral Response

Cited by 31 publications

References 134 publications

Effect of silencing Bemisia tabaci TLR3 and TOB1 on fitness and begomovirus transmission

Effect of silencing Bemisia tabaci TLR3 and TOB1 on fitness and begomovirus transmission

Aedes albopictus salivary adenosine deaminase is an immunomodulatory factor facilitating dengue virus replication

Tripartite motif-containing protein 46 accelerates influenza A H7N9 virus infection by promoting K48-linked ubiquitination of TBK1

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