Abstract
BackgroundDengue virus (DENV), the causative agent of human Dengue hemorrhagic fever, is a mosquito-borne virus found in tropical and sub-tropical regions around the world. Vaccines against DENV are currently unavailable. Guanylate-binding protein 1 (GBP1) is one of the Interferon (IFN) stimulated genes (ISGs) and has been shown important for host immune defense against various pathogens. However, the role of GBP1 during DENV infection remains unclarified. In this study, we evaluated the relevance of GBP1 to DENV infection in in vitro model.FindingsQuantitative RT-PCR (qRT-PCR) and Western blot showed that the expression of mouse Gbp1 was dramatically upregulated in DENV-infected RAW264.7 cells. The intracellular DENV loads were significantly higher in Gbp1 silenced cells compared with controls. The expression levels of selective anti-viral cytokines were decreased in Gbp1 siRNA treated cells, while the transcription factor activity of NF-κB was impaired upon GBP1 silencing during infection.ConclusionsOur data suggested that GBP1 plays an antiviral role during DENV infection.
Highlights
Dengue virus (DENV), the causative agent of human Dengue hemorrhagic fever, is a mosquito-borne virus found in tropical and sub-tropical regions around the world
Our data suggested that Guanylate-binding protein 1 (GBP1) plays an antiviral role during DENV infection
Guanylate-binding protein 1 (GBP1) is one of the interferon-stimulated genes (ISGs) that most strongly induced by IFNs [9] and belongs to a family of GTPases which are divided into three groups: (1) the large GTPases, known as GBPs; (2) the small GTPases; (3) the Mx proteins
Summary
Dengue virus (DENV), the causative agent of human Dengue hemorrhagic fever, is a mosquito-borne virus found in tropical and sub-tropical regions around the world. Conclusions: Our data suggested that GBP1 plays an antiviral role during DENV infection. Interferons (IFNs) are major antiviral cytokines released by host cells in response to viral and other pathogenic infections and play crucial roles in induction and regulation of both innate and adaptive immune responses [6].
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