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Review
. 2016 Jul;13(3):514-34.
doi: 10.1007/s13311-016-0443-5.

Encephalitic Arboviruses: Emergence, Clinical Presentation, and Neuropathogenesis

Hamid Salimi  1 , Matthew D Cain  1 , Robyn S Klein  2   3   4
Affiliations
Review

Encephalitic Arboviruses: Emergence, Clinical Presentation, and Neuropathogenesis

Hamid Salimi et al. Neurotherapeutics. 2016 Jul.

Abstract

Arboviruses are arthropod-borne viruses that exhibit worldwide distribution, contributing to systemic and neurologic infections in a variety of geographical locations. Arboviruses are transmitted to vertebral hosts during blood feedings by mosquitoes, ticks, biting flies, mites, and nits. While the majority of arboviral infections do not lead to neuroinvasive forms of disease, they are among the most severe infectious risks to the health of the human central nervous system. The neurologic diseases caused by arboviruses include meningitis, encephalitis, myelitis, encephalomyelitis, neuritis, and myositis in which virus- and immune-mediated injury may lead to severe, persisting neurologic deficits or death. Here we will review the major families of emerging arboviruses that cause neurologic infections, their neuropathogenesis and host neuroimmunologic responses, and current strategies for treatment and prevention of neurologic infections they cause.

Keywords: Arbovirus; Blood-brain barrier; Innate immunity; Viral encephalitis.

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Figures

Fig. 1
Fig. 1
Routes of arbovirus entry into the central nervous system (CNS). (A) Infection of olfactory sensory neurons (OSN) in the olfactory neuroepithelium (ONE) following intranasal inoculation or ONE infection from fenestrated vessels (FV). CNS entry occurs after viral migration through the cribiform plate (CP), subsequent infection of mitral cells (MC) at the glomeruli (G) of the olfactory bulb (OB), and dissemination along neuronal tracts. (B) Retrograde transport of virus along axon microtubules (MT) of peripheral neurons facilitates entry into the CNS at the spinal cord. (C) Virus entry through the blood–brain barrier (BBB) is dependent on transcellular transport by brain microvascular endothelial cells (BMECs) of virions or paracellular migration of virions following disruption of tight junctions (TJ). Infected leukocytes may also facilitate CNS entry via paracellular or transcellular extravasation – the “Trojan Horse” model FV = fenestrated vessel; BMEC = brain microvascular endothelial cells
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