Home HOME Acta Virologica 2018 Acta Virologica Vol.62, No.1, p.16-27, 2018

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Quarterly,
Founded: 1957
ISSN 0001-723X
E-ISSN 1336-2305

Published in English

Impact Factor = 1.82

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Acta Virologica Vol.62, No.1, p.16-27, 2018

Title: Disruption of the blood brain barrier is vital property of neurotropic viral infection of the central nervous system
Author: M. M. JAMIL AL-OBAIDI, A. BAHADORAN, S. M. WANG, R. MANIKAM, CH. S. RAJU, S. D. SEKARAN

Abstract: The blood brain barrier consisting of astrocytes, pericytes and brain microvascular endothelial cells plays a vital role in the pathogenesis of neurotropic viruses by controlling the access of circulating molecules, immune cells or viruses into the central nervous system (CNS). However, this barrier is not impenetrable and neuroviruses have evolved to disrupt and evade it. This review aims to describe the underlying entry mechanisms of several neuroviruses such as (Japanese encephalitis virus (JEV), West Nile virus (WNV), Zika virus (ZIKV), Nipah virus (NiV), Rabies virus (RABV), Herpes simplex virus (HSV) and Human immunodeficiency virus (HIV)) into the CNS through BBB disruption. The mechanisms, through which neurotropic viruses enter the BBB, are being studied and are becoming clearer, however, some aspects still remain unknown. Some of these viruses are able to invade the brain parenchyma by a ‘Trojan horse’ mechanism, through diapedesis of infected immune cells that either cross the BBB paracellularly or transcellularly. Important mechanisms of BBB disruption associated with paracellular entry of viruses include alterations in expression or phosphorylation of tight junction proteins, disruption of the basal lamina and disruption of the actin cytoskeleton. In the absence of such mechanisms, indirect effects of viruses on the immune system are likely causes of barrier disruption.

Keywords: adhesion molecules; blood-brain barrier; central nervous system; neuroviruses; tight junction
Published online: 09-Mar-2018
Year: 2018, Volume: 62, Issue: 1 Page From: 16, Page To: 27
doi:10.4149/av_2018_102


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