Journal
VIRUSES-BASEL
Volume 5, Issue 11, Pages 2643-2658Publisher
MDPI
DOI: 10.3390/v5112643
Keywords
flavivirus; pathogenesis; encephalitis; RIG-I-like receptor; Toll-like receptor; Nod-like receptor; antiviral gene; innate immunity; interferon; West Nile virus
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Funding
- NIH [U19AI057266]
- Children's Healthcare of Atlanta
- Emory Vaccine Center
- Georgia Research Alliance
- Emory University Research Committee
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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-1 beta 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.
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