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Review
. 2009 Aug;66(8):939-48.
doi: 10.1001/archneurol.2009.153.

Emerging viral infections of the central nervous system: part 1

Kenneth L Tyler  1
Affiliations
Review

Emerging viral infections of the central nervous system: part 1

Kenneth L Tyler. Arch Neurol. 2009 Aug.

Abstract

In this 2-part review, I will focus on emerging virus infections of the central nervous system (CNS). Part 1 will introduce the basic features of emerging infections, including their definition, epidemiology, and the frequency of CNS involvement. Important mechanisms of emergence will be reviewed, including viruses spreading into new host ranges as exemplified by West Nile virus (WNV), Japanese encephalitis (JE) virus, Toscana virus, and enterovirus 71 (EV71). Emerging infections also result from opportunistic spread of viruses into known niches, often resulting from attenuated host resistance to infection. This process is exemplified by transplant-associated cases of viral CNS infection caused by WNV, rabies virus, lymphocytic choriomeningitis, and lymphocytic choriomeningitis-like viruses and by the syndrome of human herpesvirus 6 (HHV6)-associated posttransplantation acute limbic encephalitis. The second part of this review begins with a discussion of JC virus and the occurrence of progressive multifocal leukoencephalopathy in association with novel immunomodulatory therapies and then continues with an overview of the risk of infection introduced by imported animals (eg, monkeypox virus) and examples of emerging diseases caused by enhanced competence of viruses for vectors and the spread of vectors (eg, chikungunya virus) and then concludes with examples of novel viruses causing CNS infection as exemplified by Nipah and Hendra viruses and bat lyssaviruses.

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Figures

Figure 1
Figure 1
Distribution of wild-type poliomyelitis cases worldwide 2008. Source: World Health Organization.
Figure 2
Figure 2
Number of cases of West Nile virus (WNV) infection reported to the Centers for Disease Control and Prevention (CDC) in 2007 (A) and 2008 (B) and incidence per million population in 2007 (C) and 2008 (D). Reproduced with permission from the CDC.
Figure 3
Figure 3
Axial proton density magnetic resonance image (left) and coronal fluid-attenuated inversion recovery magnetic resonance image of patients with West Nile virus encephalitis showing increased signal in the upper brainstem, thalamus, and basal ganglia (A) and substantia nigra of the midbrain (B).
Figure 4
Figure 4
Approximate geographic distribution of Japanese encephalitis virus. Source: copyright 2006, Massachusetts Medical Society; all rights reserved.
Figure 5
Figure 5
Axial fluid-attenuated inversion recovery magnetic resonance images at day 22 (A and B) and day 28 (C and D) in a patient with posttransplant rabies encephalitis. Day 22 images show subtle leptomeningeal and pontomesencephalic junction increased signal. Day 28 images show increased signal in anteromedial temporal lobes including hippocampi. Coronal fast spin-echo image at day 28 (E) shows diffuse anterior temporal and anterior and inferior frontal increased signal. Source: copyright 2005, American Medical Association; all rights reserved.
Figure 6
Figure 6
Axial fluid-attenuated inversion recovery (top rows) and diffusion-weighted (bottom rows) sequences in patients with human herpesvirus 6–associated posttransplant acute limbic encephalitis showing abnormal increased signal in the limbic system, including the uncus, amygdala, and anterior hippocampus in all patients. Reproduced with permission from Wolters Kluwer Health.
See this image and copyright information in PMC

References

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