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J. Virol. doi:10.1128/JVI.00236-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Retrograde axonal transport: a major transmission route of enterovirus 71 in mice

Departments of Microbiology & Immunology, Institute of Basic Medical Sciences, Medical Laboratory Science and Biotechnology, Pediatrics, College of Medicine, National Cheng Kung University, Tainan, Taiwan, Republic of China

^* To whom correspondence should be addressed. Email: dckyu{at}mail.ncku.edu.tw.

	Abstract

Inoculation of enterovirus 71 (EV71) by oral (p.o.), intramuscular (i.m.), or intracranial (i.c.) routes resulted in brain infection, flaccid paralysis, pulmonary dysfunction, and death of 7-day-old mice. The lag time of disease progression indicated that neuroinvasion from the inoculation sites was a prerequisite for the development of the clinical signs. Although EV71 p.o. inoculation led to a persistent viremia and a transient increase in blood-brain-barrier permeability at the early stage of the infection, only low levels of virus could be detected in the brain which neither led to severe infection nor clinical illness, suggesting hematogenous transport might not represent a major transmission route. In the spinal cord, following both p.o. and hindlimb i.m. inoculation, the virus first appeared and increased rapidly in the lower segments, especially at the anterior horn areas, and then spread to the upper segments and brain in the presence of viremia. A reverse pattern with the virus being first detected in the upper segment was observed when the virus was i.m. inoculated in the forelimb. Colchicine, a fast axonal transport inhibitor, but not sciatic nerve transection reduced EV71 neuroinvasion in a dose-dependent manner, indicating a neuronal transmission of the virus.

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