Zika virus replication on endothelial cells and invasion into the central nervous system by inhibiting interferon β translation

Wang, Ke; Zou, Song-Song; Chen, Haowei; Higazy, Doaa; Gao, Xiaohuan; Zhang, Yage; Cao, Shengbo; Cui, Min

doi:10.1016/j.virol.2023.03.006

Cited by 5 publications

(3 citation statements)

References 75 publications

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“…Among the other members of the Flaviviridae, ZIKV may be associated with certain hemostatic alterations, particularly in the placenta and in the umbilical cord [125,126], or may stimulate endothelial activation associated with BBB breakdown [127]. EVs may contribute to these processes.…”

Section: Zikvmentioning

confidence: 99%

Extracellular Vesicles in Flaviviridae Pathogenesis: Their Roles in Viral Transmission, Immune Evasion, and Inflammation

Latanova,

Karpov,

Starodubova

2024

IJMS

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The members of the Flaviviridae family are becoming an emerging threat for public health, causing an increasing number of infections each year and requiring effective treatment. The consequences of these infections can be severe and include liver inflammation with subsequent carcinogenesis, endothelial damage with hemorrhage, neuroinflammation, and, in some cases, death. The mechanisms of Flaviviridae pathogenesis are being actively investigated, but there are still many gaps in their understanding. Extracellular vesicles may play important roles in these mechanisms, and, therefore, this topic deserves detailed research. Recent data have revealed the involvement of extracellular vesicles in steps of Flaviviridae pathogenesis such as transmission, immune evasion, and inflammation, which is critical for disease establishment. This review covers recent papers on the roles of extracellular vesicles in the pathogenesis of Flaviviridae and includes examples of clinical applications of the accumulated data.

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Section: Zikvmentioning

confidence: 99%

Extracellular Vesicles in Flaviviridae Pathogenesis: Their Roles in Viral Transmission, Immune Evasion, and Inflammation

Latanova,

Karpov,

Starodubova

2024

IJMS

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“…When considering viral infection in MAPK pathway, it is observed that the Zika virus (ZIKV) induces ISG expressing, which subsequently increases the levels of p38 and ERK ½, promoting the secretion of chemokines that facilitate the development of viral infection and inflammation. Meanwhile, ZIKV inhibits the phosphorylation of ribosomal protein S6 (RPS6), leading to reduced IFN-β translation and a consequent increase in of inflammation levels [ 203 ]. In addition, it is noteworthy that the myxoma virus could specifically activate ERK1/2 signaling, thereby promoting the increased secretion of IFN-α and IFN-β that resist viral infection and expansion of inflammation [ 202 ].…”

Section: Type I Interferon Signaling In Inflammationmentioning

confidence: 99%

The crucial regulatory role of type I interferon in inflammatory diseases

Ji,

Li,

Chen

et al. 2023

Cell Biosci

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Type I interferon (IFN-I) plays crucial roles in the regulation of inflammation and it is associated with various inflammatory diseases including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and periodontitis, impacting people's health and quality of life. It is well-established that IFN-Is affect immune responses and inflammatory factors by regulating some signaling. However, currently, there is no comprehensive overview of the crucial regulatory role of IFN-I in distinctive pathways as well as associated inflammatory diseases. This review aims to provide a narrative of the involvement of IFN-I in different signaling pathways, mainly mediating the related key factors with specific targets in the pathways and signaling cascades to influence the progression of inflammatory diseases. As such, we suggested that IFN-Is induce inflammatory regulation through the stimulation of certain factors in signaling pathways, which displays possible efficient treatment methods and provides a reference for the precise control of inflammatory diseases.

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“…Human immunodeficiency viruses (HIVs), different flaviviruses, and new-world alphaviruses have also been studied for BBB penetration and CNS infection in vitro [ 201 , 256 ]. Several studies showed the ability of the Zika virus and other flaviviruses in terms of infecting and activating BMECs [ 257 , 258 , 259 , 260 , 261 , 262 ]. Moreover, the virus crossed the BBB via transcytosis without significantly increasing permeability [ 258 , 259 , 260 ].…”

Section: Disease-specific Modeling Of Neuroinflammationmentioning

confidence: 99%

Blood–Brain Barrier Breakdown in Neuroinflammation: Current In Vitro Models

Brandl,

Reindl

2023

IJMS

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The blood–brain barrier, which is formed by tightly interconnected microvascular endothelial cells, separates the brain from the peripheral circulation. Together with other central nervous system-resident cell types, including pericytes and astrocytes, the blood–brain barrier forms the neurovascular unit. Upon neuroinflammation, this barrier becomes leaky, allowing molecules and cells to enter the brain and to potentially harm the tissue of the central nervous system. Despite the significance of animal models in research, they may not always adequately reflect human pathophysiology. Therefore, human models are needed. This review will provide an overview of the blood–brain barrier in terms of both health and disease. It will describe all key elements of the in vitro models and will explore how different compositions can be utilized to effectively model a variety of neuroinflammatory conditions. Furthermore, it will explore the existing types of models that are used in basic research to study the respective pathologies thus far.

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Zika virus replication on endothelial cells and invasion into the central nervous system by inhibiting interferon β translation

Cited by 5 publications

References 75 publications

Extracellular Vesicles in Flaviviridae Pathogenesis: Their Roles in Viral Transmission, Immune Evasion, and Inflammation

Extracellular Vesicles in Flaviviridae Pathogenesis: Their Roles in Viral Transmission, Immune Evasion, and Inflammation

The crucial regulatory role of type I interferon in inflammatory diseases

Blood–Brain Barrier Breakdown in Neuroinflammation: Current In Vitro Models

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