Viral interactions with the blood-brain barrier: old dog, new tricks

  title={Viral interactions with the blood-brain barrier: old dog, new tricks},
  author={Jianghui Hou and Lane A. Baker and Lushan Zhou and Robyn S. Klein},
  journal={Tissue Barriers},
Brain endothelial cells form a unique cellular structure known as the tight junction to regulate the exchanges between the blood and the parenchyma by limiting the paracellular diffusion of blood-borne substance. Together with the restricted pathway of transcytosis, the tight junction in the brain endothelial cells provides the central nervous system (CNS) with effective protection against both the foreign pathogens and the host immune cells, which is also termed the “blood-brain barrier.” The… 
Introduction for the Special Issue on the Blood-Brain Barrier
This Special Issue of Tissue Barriers is dedicated to the Blood-Brain Barrier and contains 11 reviews that altogether summarize and discuss recent advances in understanding normal structure, development and functions of the BBB and the mechanisms underlying disruption of this barrier in CNS diseases.
Dengue Virus Infection of Blood–Brain Barrier Cells: Consequences of Severe Disease
Evidence of the BBB cell infection with DENV and the response established toward it by these cells is presented and the consequences of this response on the nervous tissue are described, and the complexity and unpredictability of dengue and the neurological alterations induced by it are shown.
Genetic disruption of the Blood Brain Barrier leads to protective barrier formation at the Glia Limitans
Genetic disruption of the BBB generates endothelial signals capable of driving the implementation of a secondary barrier at the Glia Limitans to protect the parenchyma, which has implications for treatment strategies in the acute and chronic phases of multiple sclerosis pathophysiology.
Viruses in human central nervous system — invasion, transmission, and latency: a literature review
An understanding of the molecular mechanisms controlling the spread of viruses in the nervous system is not formed and severe pathology is developed in case of insufficiency of aggregate response to viral invasion.
Ethnicity and the relationship between covid-19 and the herpes simplex viruses
  • P. Bond
  • Medicine
    Medical Hypotheses
  • 2021
The Causes and Long-Term Consequences of Viral Encephalitis
How viruses can reach the brain, the impact of viral encephalitis on brain function, and the neurocognitive sequelae reported even after viral clearance are discussed are discussed.
PERK Is Critical for Alphavirus Nonstructural Protein Translation
The data indicate that PERK is an essential factor for the translation of alphavirus nonstructural proteins and impacts multiple RNA viruses, making it an exciting target for antiviral development.
Blood–brain barrier genetic disruption leads to protective barrier formation at the Glia Limitans
Results provide evidence for the novel concept of “chronic neuroinflammatory tolerance” in which BBB opening in the resting state is sufficient to stimulate a protective barrier at the Glia Limitans that limits the severity of subsequent neuroinflammatory disease.


Viral sensing at the blood–brain barrier: New roles for innate immunity at the CNS vasculature
Recent advances in understanding how BBB function governs both viral pathogenesis and host immune responses during neurotropic viral infections are summarized.
Size-selective loosening of the blood-brain barrier in claudin-5–deficient mice
In claudin-5–deficient mice, the size-selective loosening of the blood-brain barrier was selectively affected, which provides new insight into the basic molecular physiology of BBB and opens a new way to deliver potential drugs across the BBB into the central nervous system.
Association of FAK activation with lentivirus-induced disruption of blood-brain barrier tight junction-associated ZO-1 protein organization
It is demonstrated that disruption of tight junctions between BMECs is mediated through activation of focal adhesion kinase (FAK) by phosphorylation at TYR-397, and it may be possible to inhibit the development of HIVE by using inhibitors of FAK.
Blood–brain barrier disruption in simian immunodeficiency virus encephalitis
It is demonstrated that tight junction disruption occurs in SIV‐infected macaques with encephalitis in association with perivascular macrophage accumulation, and disruptions in BBB integrity could serve as portals for additional accumulation of periv vascular macrophages in SIVE.
Interferon-λ restricts West Nile virus neuroinvasion by tightening the blood-brain barrier
An indirect antiviral function of interferon-λ is established in which noncanonical signaling through IFNLR1 tightens the blood-brain barrier and restricts viral neuroinvasion and pathogenesis.
West Nile virus-induced disruption of the blood-brain barrier in mice is characterized by the degradation of the junctional complex proteins and increase in multiple matrix metalloproteinases.
It is proposed that WNV initially enters CNS without altering the BBB integrity and later virus replication in the brain initiates BBB disruption, allowing enhanced infiltration of immune cells and contribute to virus neuroinvasion via the 'Trojan-horse' route.
Rapid Remodeling of Tight Junctions during Paracellular Diapedesis in a Human Model of the Blood–Brain Barrier
It is shown that endothelial tight junctions expressing claudin-5 are dynamic and undergo rapid remodeling during TEM and suggest that tight junitions are more dynamic than previously appreciated.
HIV-1 gp120 Proteins Alter Tight Junction Protein Expression and Brain Endothelial Cell Permeability: Implications for the Pathogenesis of HIV-Associated Dementia
It is demonstrated that HIV gp120 proteins alter both the functional and molecular properties of the BBB, which could increase trafficking of HIV, infected cells, and toxic humoral factors into the central nervous system and contribute to the pathogenesis of HAD.