Flavivirus and its Threat

2021 ◽  
Author(s):  
Satashree Paul
Keyword(s):  
Endothelial Cells ◽  
Nervous System ◽  
Cell Migration ◽  
Blood Brain Barrier ◽  
Immune Cell ◽  
Structure And Function ◽  
Brain Barrier ◽  
Target Cells ◽  
Immune Cell Migration ◽  
And Function

A number of studies found that the virus can activate the endothelial cells and affect the structure and function of the blood?brain barrier, promoting immune cell migration to benefit the virus nervous system target cells infected by flaviviruses.

scholarly journals 2-Photon Microscopy Imaging of Immune Cell Migration Across the Blood-Brain Barrier in the Spine During Induction of Acute Chronic Injury

2011 ◽  
Vol 17 (S2) ◽  
pp. 76-77
Author(s):  
Y Othman ◽  
D Barkauskas ◽  
T Evans ◽  
J Silver ◽  
A Huang
Keyword(s):  
Cell Migration ◽  
Blood Brain Barrier ◽  
Immune Cell ◽  
Brain Barrier ◽  
Chronic Injury ◽  
Microscopy Imaging ◽  
Blood Brain ◽  
Immune Cell Migration

Extended abstract of a paper presented at Microscopy and Microanalysis 2011 in Nashville, Tennessee, USA, August 7–August 11, 2011.

scholarly journals Delivery of Therapeutic Agents to the Central Nervous System and the Promise of Extracellular Vesicles

Pharmaceutics ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 492
Author(s):  
Charlotte A. René ◽  
Robin J. Parks
Keyword(s):  
Central Nervous System ◽  
Endothelial Cells ◽  
Nervous System ◽  
Blood Brain Barrier ◽  
Extracellular Vesicles ◽  
Therapeutic Agents ◽  
Target Cells ◽  
Significant Barrier ◽  
The Central Nervous System ◽  
Delivery Vehicles

The central nervous system (CNS) is surrounded by the blood–brain barrier (BBB), a semipermeable border of endothelial cells that prevents pathogens, solutes and most molecules from non-selectively crossing into the CNS. Thus, the BBB acts to protect the CNS from potentially deleterious insults. Unfortunately, the BBB also frequently presents a significant barrier to therapies, impeding passage of drugs and biologicals to target cells within the CNS. This review provides an overview of different approaches to deliver therapeutics across the BBB, with an emphasis in extracellular vesicles as delivery vehicles to the CNS.

Structure and function of the blood–brain barrier

2010 ◽  
Vol 37 (1) ◽  
pp. 13-25 ◽  
Author(s):  
N. Joan Abbott ◽  
Adjanie A.K. Patabendige ◽  
Diana E.M. Dolman ◽  
Siti R. Yusof ◽  
David J. Begley
Keyword(s):  
Blood Brain Barrier ◽  
Structure And Function ◽  
Brain Barrier ◽  
Blood Brain ◽  
And Function

Overview of the Structure and Function of the Blood-Brain Barrier in vivo

2001 ◽  
pp. 1-7 ◽  
Author(s):  
Joseph D. Fenstermacher ◽  
Tavarekere Nagaraja ◽  
Kenneth R. Davies
Keyword(s):  
Blood Brain Barrier ◽  
Structure And Function ◽  
Brain Barrier ◽  
Blood Brain ◽  
And Function

scholarly journals Encephalitic Alphaviruses Exploit Caveola-Mediated Transcytosis at the Blood-Brain Barrier for Central Nervous System Entry

mBio ◽  
2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Hamid Salimi ◽  
Matthew D. Cain ◽  
Xiaoping Jiang ◽  
Robyn A. Roth ◽  
Wandy L. Beatty ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Endothelial Cells ◽  
Nervous System ◽  
Viral Replication ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Type I ◽  
Brain Endothelial Cells ◽  
Blood Brain ◽  
Deficient Mice

ABSTRACT Venezuelan and western equine encephalitis viruses (VEEV and WEEV, respectively) invade the central nervous system (CNS) early during infection, via neuronal and hematogenous routes. While viral replication mediates host shutoff, including expression of type I interferons (IFN), few studies have addressed how alphaviruses gain access to the CNS during established infection or the mechanisms of viral crossing at the blood-brain barrier (BBB). Here, we show that hematogenous dissemination of VEEV and WEEV into the CNS occurs via caveolin-1 (Cav-1)-mediated transcytosis (Cav-MT) across an intact BBB, which is impeded by IFN and inhibitors of RhoA GTPase. Use of reporter and nonreplicative strains also demonstrates that IFN signaling mediates viral restriction within cells comprising the neurovascular unit (NVU), differentially rendering brain endothelial cells, pericytes, and astrocytes permissive to viral replication. Transmission and immunoelectron microscopy revealed early events in virus internalization and Cav-1 association within brain endothelial cells. Cav-1-deficient mice exhibit diminished CNS VEEV and WEEV titers during early infection, whereas viral burdens in peripheral tissues remained unchanged. Our findings show that alphaviruses exploit Cav-MT to enter the CNS and that IFN differentially restricts this process at the BBB. IMPORTANCE VEEV, WEEV, and eastern equine encephalitis virus (EEEV) are emerging infectious diseases in the Americas, and they have caused several major outbreaks in the human and horse population during the past few decades. Shortly after infection, these viruses can infect the CNS, resulting in severe long-term neurological deficits or death. Neuroinvasion has been associated with virus entry into the CNS directly from the bloodstream; however, the underlying molecular mechanisms have remained largely unknown. Here, we demonstrate that following peripheral infection alphavirus augments vesicular formation/trafficking at the BBB and utilizes Cav-MT to cross an intact BBB, a process regulated by activators of Rho GTPases within brain endothelium. In vivo examination of early viral entry in Cav-1-deficient mice revealed significantly lower viral burdens in the brain than in similarly infected wild-type animals. These studies identify a potentially targetable pathway to limit neuroinvasion by alphaviruses.

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