Abstract
The innate immune system is the host’s first line of defense against the invasion of pathogens including flavivirus. The programmed cell death controlled by genes plays an irreplaceable role in resisting pathogen invasion and preventing pathogen infection. However, the inflammatory cell death, which can trigger the overflow of a large number of pro-inflammatory cytokines and cell contents, will initiate a severe inflammatory response. In this review, we summarized the current understanding of the innate immune response, inflammatory cell death pathway and cytokine secretion regulation during Dengue virus, West Nile virus, Zika virus, Japanese encephalitis virus and other flavivirus infections. We also discussed the impact of these flavivirus and viral proteins on these biological processes. This not only provides a scientific basis for elucidating the pathogenesis of flavivirus, but also lays the foundation for the development of effective antiviral therapies.
Highlights
Reviewed by: Xin Li, China Agricultural University, China Bhesh Raj Sharma, St
We summarized the current understanding of the innate immune response, inflammatory cell death pathway and cytokine secretion regulation during Dengue virus, West Nile virus, Zika virus, Japanese encephalitis virus and other flavivirus infections
Signal transduction mediated by Toll-like receptors (TLRs) and retinoic acid-inducible gene Ilike receptors (RLRs) results in the secretion of type I interferon (IFN-I), which subsequently stimulates the expression of IFN-stimulating genes (ISGs) to establish an antiviral state [24,25,26]
Summary
As the first hurdle to protect the host from microbial invasion, the innate immune system can establish a rapid, broadly response to control infection, and plays a key role in the establishment of an adaptive immune response, which can lead to pathogen-specific and durable. When dealing with specific danger-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs), members of the NLRs family are able to assemble large multiprotein complexes called inflammasomes [2]. The priming step is induced by TLRs and cytokine receptors, such as the tumor necrosis factor receptor (TNFR) or IL-1 receptor (IL-1R), which recognize PAMPs or DAMPs and upregulate the transcription of NLRP3 and IL-1b. PAMPs and DAMPs promote NLRP3 inflammasome assembly. Innate immune response and inflammasome activation are recognized key obstacles in the process of virus invasion. The initiation of the innate immune response needs to be strictly regulated, since excessive activation could cause harmful tissue damage and systemic inflammation [8]. Thence, the balance regulation between host’s innate immune responses and virus invasion is considered as a potential method for the treatment of viral infection. The balance should be well regulated to maintain antiviral function and avoid excessive inflammation
Sign-in/Register to view highlights & summary 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.
