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1.
Virology ; 487: 1-10, 2016 Jan.
Article in English | MEDLINE | ID: mdl-26479325

ABSTRACT

Neurotropic viruses initiate infection in peripheral tissues prior to entry into the central nervous system (CNS). However, mechanisms of dissemination are not completely understood. We used genetically marked viruses to compare dissemination of poliovirus, yellow fever virus 17D (YFV-17D), and reovirus type 3 Dearing in mice from a hind limb intramuscular inoculation site to the sciatic nerve, spinal cord, and brain. While YFV-17D likely entered the CNS via blood, poliovirus and reovirus likely entered the CNS by transport through the sciatic nerve to the spinal cord. We found that dissemination was inefficient in adult immune-competent mice for all three viruses, particularly reovirus. Dissemination of all viruses was more efficient in immune-deficient mice. Although poliovirus and reovirus both accessed the CNS by transit through the sciatic nerve, stimulation of neuronal transport by muscle damage enhanced dissemination only of poliovirus. Our results suggest that these viruses access the CNS using different pathways.


Subject(s)
Central Nervous System/virology , Orthoreovirus, Mammalian/pathogenicity , Peripheral Nerves/virology , Poliovirus/pathogenicity , Yellow fever virus/pathogenicity , Animals , Cell Line , Cricetinae , HeLa Cells , Humans , Interferon Type I/immunology , Mice , Mice, Inbred C57BL , Mice, Knockout , Orthoreovirus, Mammalian/growth & development , Poliomyelitis/pathology , Poliomyelitis/transmission , Poliovirus/growth & development , Receptor, Interferon alpha-beta/genetics , Reoviridae Infections/pathology , Reoviridae Infections/transmission , Sciatic Nerve/virology , Yellow Fever/pathology , Yellow Fever/transmission , Yellow fever virus/growth & development
2.
Cell Host Microbe ; 11(5): 420-1, 2012 May 17.
Article in English | MEDLINE | ID: mdl-22607794

ABSTRACT

Mitochondria are dynamic organelles with many functions. In this issue of Cell Host & Microbe, Kramer and Enquist (2012) show that mitochondrial motility and morphology are disrupted during alphaherpesvirus infection, which aids viral replication and transport in neurons.

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