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<a href="http://doi.org/10.1006/viro.2001.1299" target="_blank" rel="noreferrer noopener">http://doi.org/10.1006/viro.2001.1299</a>
Pages
262–272
Issue
2
Volume
293
Dublin Core
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Title
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Reexamination of amphotropic murine leukemia virus neurovirulence: neural stem cell-mediated microglial infection fails to induce acute neurodegeneration.
Publisher
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Virology
Date
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2002
2002-02
Subject
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*Leukemia Virus; *Reassortant Viruses/pathogenicity; Animals; Cell Line; Central Nervous System Diseases/*pathology/virology; Experimental/*pathology; Friend murine leukemia virus/genetics/pathogenicity; Leukemia; Mice; Microglia/pathology/virology; Murine/isolation & purification/pathogenicity; Newborn; Retroviridae Infections/*pathology; Tumor Virus Infections/*pathology; Viral Envelope Proteins/genetics/isolation & purification; Viremia; Virulence
Creator
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Traister Russell S; Lynch William P
Description
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The 4070A amphotropic murine leukemia virus (A-MuLV) has been variably reported to harbor neurovirulence determinants within its env gene. In this report we reexamined this issue by applying two approaches previously demonstrated to amplify murine leukemia virus neurovirulence. The first approach involved introducing the 4070A env gene into the background of Friend virus clone FB29 to enhance peripheral virus replication kinetics and central nervous system entry. The resulting chimeric virus, FrAmE, exhibited widespread vascular infection throughout the central nervous system (CNS); however, parenchymal infection was quite limited. Neither clinical neurological signs nor spongiform neurological changes accompanied FrAmE CNS infection. To overcome this CNS entry limitation, 4070A and FrAmE were delivered directly into the CNS via transplantation of infected C17.2 neural stem cells (NSCs). Significantly, NSC dissemination of either 4070A or FrAmE resulted in widespread, high-level amphotropic virus expression within the CNS parenchyma, including the infection of microglia, the critical target required for inducing neurodegeneration. Despite the extensive CNS infection, no associated clinical neurological signs or acute neuropathological changes were observed. Interestingly, we observed the frequent appearance of circulating polytropic (MCF) virus in the serum of amphotropic virus-infected animals. However, neither peripheral inoculation of an amphotropic/MCF virus mixture nor transplantation of NSCs expressing both amphotropic and MCF viruses induced acute clinical neurological signs or spongiform neuropathology. Thus, the results generated in this study suggest that the 4070A env gene is not inherently neurovirulent. However, the frequent appearance of endogenous MCF viruses suggests the possibility that the interactions of amphotropic viruses with endogenous retroviral elements could contribute to the development of retrovirus-induced neurodegenerative disease.
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<a href="http://doi.org/10.1006/viro.2001.1299" target="_blank" rel="noreferrer noopener">10.1006/viro.2001.1299</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Leukemia Virus
*Reassortant Viruses/pathogenicity
2002
Animals
Cell Line
Central Nervous System Diseases/*pathology/virology
Department of Integrative Medical Sciences
Experimental/*pathology
Friend murine leukemia virus/genetics/pathogenicity
Leukemia
Lynch William P
Mice
Microglia/pathology/virology
Murine/isolation & purification/pathogenicity
NEOMED College of Medicine
Newborn
Retroviridae Infections/*pathology
Traister Russell S
Tumor Virus Infections/*pathology
Viral Envelope Proteins/genetics/isolation & purification
Viremia
Virology
Virulence