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Selective passage nevertheless exists as small lipophilic molecules, cytokines, and cells of the immune system can cross the BBB using different mechanisms such as transcytosis through receptor-mediated endocytosis, transport with efflux/influx pumps, transcellular lipophilic pathways, and transcellular diapedesis. Endothelial cells are closely interacting through tight and adherens junctions (TJ and AJ respectively), which ensure the (relative) impermeability of the barrier, although anatomical sites, such as the choroid plexus (CP), are more vulnerable due to their loose inter-endothelial cell junctions.
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It is formed by closely interacting cells, which form the neurovascular unit (NVU): vascular endothelial cells that actually form the barrier, pericytes, astrocytes, and neurons (Fig. Notably, the blood brain barrier (BBB) is a tight endothelium that physically separates systemic circulation from the parenchyma. To reach the central and peripheral nervous systems (PNS), pathogens have been selected throughout evolution for their ability to interact with various barriers and machineries. This can be done directly through pathogen-mediated effects on neurons, or indirectly through inflammation-associated mechanisms when glial cells are affected for instance. This however does not exclude that some toxins, viruses, bacteria, or parasites can access this organ and cause mild to severe impairment. ĭue to its peculiar architecture, the central nervous system (CNS) is relatively protected from toxic and pathogenic factors that can be found in the blood, and in this light, it is considered as immune-privileged. “Hit and run” mechanisms leading to progressive neuronal pathology may be also considered, such as subacute sclerosing panencephalitis, a rare progressive neurological disease caused by complications associated with measles virus infection, which can have major impact including behavioral impairment cognitive decline and seizures. Notably, both viruses were found to induce significant cognitive impairment in the general population and were also proposed to be involved in the etiology of AD. Another example is found among members of the Herpesviridae family, such as cytomegalovirus (CMV), which can be associated with neurodevelopmental defects, as well as herpes simplex virus 1 (HSV-1), which induces latent infection in the nervous system and in some cases can trigger encephalitis when reactivated. HIV nervous system infection may also be linked to the etiology of some brain disorders such as amyotrophic lateral sclerosis or Alzheimer’s disease (AD).
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For example, around 50% of human immunodeficiency virus (HIV)-infected patients are suffering from mild to severe neurological impairments in a syndrome called HIV-associated neurocognitive disorder (HAND) consisting of a range of cognitive deficits such as memory and attention disorders, motor and sensory impairment, mood and behavior changes and, in some extreme cases, dementia or HAD (HIV-associated dementia). Once in the brain, altered neuronal homeostasis triggered by long-term inflammatory microenvironment and/or viral replication can have dramatic effects and lead to cognitive disorders. Accumulating evidence illustrate now the fact that neurotropic viruses have developed numerous strategies to invade the brain and, depending on the mode of entry, cellular tropism and mechanism of infection, trigger a wide range of neuronal symptoms, which can lead in some cases to severe cognitive impairments.