Abstract
We showed previously that Theiler's virus, a neurotropic non-enveloped picornavirus of mouse, traffics from the axon of infected neurons into the surrounding myelin. When this traffic is interrupted, as in the shiverer mouse which bears a mutation in the myelin basic protein gene, the virus is unable to persist in the central nervous system. In the present work, we used the Wlds mutant mouse, a strain in which axonal degeneration is considerably slowed down, to show that axon to myelin traffic takes place in the absence of axon degeneration. Our results suggest the existence of a mechanism of transfer of axonal cytoplasm into the myelin which Theiler's virus might exploit to ensure its persistence.
Highlights
Myelin is an extension of the oligodendrocyte cell body wrapped many times around the axon
In a previous paper we showed that TMEV infects retinal ganglion neurons when injected in the eye, is transported axonally in the optic nerve, and infects optic nerve oligodendrocytes through their myelin sheaths [4]
In the present work we investigated the role of axon lysis in the entry of TMEV into the myelin using the Wlds mouse, a mutant strain in which axonal degeneration is 10 times slower than in wild type controls [7]
Summary
Myelin is an extension of the oligodendrocyte cell body wrapped many times around the axon. Inactivating the Cnp myelin gene does not alter myelin ultrastructure but causes accumulation of membranous organelles in the axons, axon swelling and degeneration [2] This support role, and the exact way by which oligodendrocytes and axons communicate, is still poorly understood. We showed that a deletion of the myelin basic protein gene prevents this axon-myelin traffic and renders the mice resistant to persistent infection [4,5] This observation raises important questions regarding the mechanism of axon to myelin traffic and the role of this traffic in viral persistence. Picornaviruses, such as TMEV, are non-enveloped and cannot travel from cell to cell by budding followed by fusion. We show that TMEV enters the myelin even when the axons do not degenerate
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