Abstract
West Nile virus (WNV) is an emerging mosquito-borne flavivirus that causes annual epidemics of encephalitic disease throughout the world. Despite the ongoing risk to public health, no approved vaccines or therapies exist for use in humans to prevent or combat WNV infection. The innate immune response is critical for controlling WNV replication, limiting virus-induced pathology, and programming protective humoral and cell-mediated immunity to WNV infection. The RIG-I like receptors, Toll-like receptors, and Nod-like receptors detect and respond to WNV by inducing a potent antiviral defense program, characterized by production of type I IFN, IL-1β and expression of antiviral effector genes. Recent research efforts have focused on uncovering the mechanisms of innate immune sensing, antiviral effector genes that inhibit WNV, and countermeasures employed by WNV to antagonize innate immune cellular defenses. In this review, we highlight the major research findings pertaining to innate immune regulation of WNV infection.
Highlights
West Nile Virus is a Serious Public Health ConcernWest Nile virus (WNV) is a member of the Japanese Encephalitis virus (JEV) antigenic complex, which includes JEV, St. Louis Encephalitis, Murray Valley Encephalitis, and other neurotropic mosquito-borne flaviviruses, that combined, are major causes of virus-induced encephalitis throughout the world [1]
TLR3 and TLR7 bind to non-self RNA to trigger IRF-3, IRF-7, and NF- B dependent gene expression; (C) NLPR3 interacts with ASC, leading to caspase-1 activation and IL-1β processing; (D) Secreted type I IFN leads to formation of the interferon-stimulated gene factor 3 (ISGF3) complex that translocates to the nucleus and induces expression of interferon-stimulated response element (ISRE)-dependent genes, including IRF-7, IFN-α subtypes, and interferon-stimulated genes (ISGs)
Differential gene expression between these two neuronal subsets was linked to epigenetic modification and regulation by microRNAs. These results reveal the complexities of innate immune signaling during virus infection and underscore the importance of understanding the cell- and tissue-specific regulation of innate immune responses
Summary
West Nile virus (WNV) is a member of the Japanese Encephalitis virus (JEV) antigenic complex, which includes JEV, St. Louis Encephalitis, Murray Valley Encephalitis, and other neurotropic mosquito-borne flaviviruses, that combined, are major causes of virus-induced encephalitis throughout the world [1]. Since its introduction into the United States in 1999, WNV has caused over three million infections resulting in over 37,000 confirmed cases and 1,500 deaths [2]. In Europe, annual outbreaks of lineage 1 WNV infections have recently been compounded by the emergence of a pathogenic lineage 2 WNV strain, raising a new threat from a strain that has traditionally been nonpathogenic in humans [3]. Despite the ongoing risk to public health, there are still no approved specific therapeutics or vaccines for use in humans to combat or prevent WNV infection
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
