Interleukins, Chemokines, and Tumor Necrosis Factor Superfamily Ligands in the Pathogenesis of West Nile Virus Infection.

Authors

Emna Benzarti
Kristy O Murray
Shannon E Ronca

Publication Date

3-22-2023

Journal

Viruses

DOI

10.3390/v15030806

PMID

36992514

PMCID

PMC10053297

PubMedCentral® Posted Date

3-22-2023

PubMedCentral® Full Text Version

Post-print

Published Open-Access

yes

Keywords

Humans, Mice, Animals, West Nile Fever, Tumor Necrosis Factors, West Nile virus, Cytokines, Chemokines, Interleukins, West Nile virus, cytokines, interleukins, chemokines, tumor necrosis factor superfamily ligands, infection model

Abstract

West Nile virus (WNV) is a mosquito-borne pathogen that can lead to encephalitis and death in susceptible hosts. Cytokines play a critical role in inflammation and immunity in response to WNV infection. Murine models provide evidence that some cytokines offer protection against acute WNV infection and assist with viral clearance, while others play a multifaceted role WNV neuropathogenesis and immune-mediated tissue damage. This article aims to provide an up-to-date review of cytokine expression patterns in human and experimental animal models of WNV infections. Here, we outline the interleukins, chemokines, and tumor necrosis factor superfamily ligands associated with WNV infection and pathogenesis and describe the complex roles they play in mediating both protection and pathology of the central nervous system during or after virus clearance. By understanding of the role of these cytokines during WNV neuroinvasive infection, we can develop treatment options aimed at modulating these immune molecules in order to reduce neuroinflammation and improve patient outcomes.