1
40
5
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1128/JVI.00392-13" target="_blank" rel="noreferrer noopener">http://doi.org/10.1128/JVI.00392-13</a>
Pages
8372–8387
Issue
15
Volume
87
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Unique N-linked glycosylation of CasBrE Env influences its stability, processing, and viral infectivity but not its neurotoxicity.
Publisher
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Journal of virology
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013-08
Subject
The topic of the resource
*Protein Processing; Animals; Canavan Disease/pathology/virology; DNA Mutational Analysis; env/genetics/*metabolism; Gene Products; Glycosylation; Leukemia Virus; Mice; Murine/genetics/*pathogenicity/*physiology; Post-Translational; Virulence; Virus Replication
Creator
An entity primarily responsible for making the resource
Renszel Krystal M; Traister Russell S; Lynch William P
Description
An account of the resource
The envelope protein (Env) from the CasBrE murine leukemia virus (MLV) can cause acute spongiform neurodegeneration analogous to that induced by prions. Upon central nervous system (CNS) infection, Env is expressed as multiple isoforms owing to differential asparagine (N)-linked glycosylation. Because
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1128/JVI.00392-13" target="_blank" rel="noreferrer noopener">10.1128/JVI.00392-13</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).
*Protein Processing
2013
Animals
Canavan Disease/pathology/virology
Department of Integrative Medical Sciences
DNA Mutational Analysis
env/genetics/*metabolism
Gene Products
Glycosylation
Journal of virology
Leukemia Virus
Lynch William P
Mice
Murine/genetics/*pathogenicity/*physiology
NEOMED College of Medicine
Post-Translational
Renszel Krystal M
Traister Russell S
Virulence
Virus Replication
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1128/JVI.02210-10" target="_blank" rel="noreferrer noopener">http://doi.org/10.1128/JVI.02210-10</a>
Pages
2060–2078
Issue
5
Volume
85
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Retrovirus-induced spongiform neurodegeneration is mediated by unique central nervous system viral targeting and expression of env alone.
Publisher
An entity responsible for making the resource available
Journal of virology
Date
A point or period of time associated with an event in the lifecycle of the resource
2011
2011-03
Subject
The topic of the resource
Animals; Cell Line; Friend murine leukemia virus/genetics/metabolism; Humans; Leukemia Virus; Mice; Murine/genetics/*metabolism/pathogenicity; Nerve Degeneration; Neural Stem Cells/pathology/virology; Neurodegenerative Diseases/pathology/*virology; Retroviridae Infections/pathology/*virology; Viral Envelope Proteins/genetics/*metabolism; Virulence
Creator
An entity primarily responsible for making the resource
Li Ying; Cardona Sandra M; Traister Russell S; Lynch William P
Description
An account of the resource
Certain murine leukemia viruses (MLVs) can induce progressive noninflammatory spongiform neurodegeneration similar to that caused by prions. The primary MLV determinants responsible have been mapped to within the env gene; however, it has remained unclear how env mediates disease, whether non-Env viral components are required, and what central nervous system (CNS) cells constitute the critical CNS targets. To address these questions, we examined the effect of transplanting engraftable C17.2 neural stem cells engineered to pseudotype, disseminate, and trans-complement neurovirulent (CasBrE, CasE, and CasES) or non-neurovirulent (Friend and SFF-FE) env sequences (SU or SU/TM) within the CNS using either the "non-neurovirulent" amphotropic helper virus, 4070A, or pgag-polgpt (a nonpackaged vector encoding Gag-Pol). These studies revealed that acute
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1128/JVI.02210-10" target="_blank" rel="noreferrer noopener">10.1128/JVI.02210-10</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2011
Animals
Cardona Sandra M
Cell Line
Department of Integrative Medical Sciences
Friend murine leukemia virus/genetics/metabolism
Humans
Journal of virology
Leukemia Virus
Li Ying
Lynch William P
Mice
Murine/genetics/*metabolism/pathogenicity
NEOMED College of Medicine
Nerve Degeneration
Neural Stem Cells/pathology/virology
Neurodegenerative Diseases/pathology/*virology
Retroviridae Infections/pathology/*virology
Traister Russell S
Viral Envelope Proteins/genetics/*metabolism
Virulence
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1128/JVI.03156-15" target="_blank" rel="noreferrer noopener">http://doi.org/10.1128/JVI.03156-15</a>
Pages
3385–3399
Issue
7
Volume
90
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Ecotropic Murine Leukemia Virus Infection of Glial Progenitors Interferes with Oligodendrocyte Differentiation: Implications for Neurovirulence.
Publisher
An entity responsible for making the resource available
Journal of virology
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-01
Subject
The topic of the resource
3T3 Cells; Animals; Cell Line; Cell Proliferation; Cell Survival; env/biosynthesis; Female; Gene Products; Leukemia Virus; Male; Mice; Motor Neuron Disease/*virology; Murine/*pathogenicity; Neural Stem Cells/*virology; Neurogenesis/*physiology; Neuroglia/*virology; Oligodendroglia/cytology/virology; Retroviridae Infections/*complications; Transgenic
Creator
An entity primarily responsible for making the resource
Li Ying; Dunphy Jaclyn M; Pedraza Carlos E; Lynch Connor R; Cardona Sandra M; Macklin Wendy B; Lynch William P
Description
An account of the resource
UNLABELLED: Certain murine leukemia viruses (MLVs) are capable of inducing fatal progressive spongiform motor neuron disease in mice that is largely mediated by viral Env glycoprotein expression within central nervous system (CNS) glia. While the etiologic mechanisms and the glial subtypes involved remain unresolved, infection of NG2 glia was recently observed to correlate spatially and temporally with altered neuronal physiology and spongiogenesis. Since one role of NG2 cells is to serve as oligodendrocyte (OL) progenitor cells (OPCs), we examined here whether their infection by neurovirulent (FrCasE) or nonneurovirulent (Fr57E) ecotropic MLVs influenced their viability and/or differentiation. Here, we demonstrate that OPCs, but not OLs, are major CNS targets of both FrCasE and Fr57E. We also show that MLV infection of neural progenitor cells (NPCs) in culture did not affect survival, proliferation, or OPC progenitor marker expression but suppressed certain glial differentiation markers. Assessment of glial differentiation in vivo using transplanted transgenic NPCs showed that, while MLVs did not affect cellular engraftment or survival, they did inhibit OL differentiation, irrespective of MLV neurovirulence. In addition, in chimeric brains, where FrCasE-infected NPC transplants caused neurodegeneration, the transplanted NPCs proliferated. These results suggest that MLV infection is not directly cytotoxic to OPCs but rather acts to interfere with OL differentiation. Since both FrCasE and Fr57E viruses restrict OL differentiation but only FrCasE induces overt neurodegeneration, restriction of OL maturation alone cannot account for neuropathogenesis. Instead neurodegeneration may involve a two-hit scenario where interference with OPC differentiation combined with glial Env-induced neuronal hyperexcitability precipitates disease. IMPORTANCE: A variety of human and animal retroviruses are capable of causing central nervous system (CNS) neurodegeneration manifested as motor and cognitive deficits. These retroviruses infect a variety of CNS cell types; however, the specific role each cell type plays in neuropathogenesis remains to be established. The NG2 glia, whose CNS functions are only now emerging, are a newly appreciated viral target in murine leukemia virus (MLV)-induced neurodegeneration. Since one role of NG2 glia is that of oligodendrocyte progenitor cells (OPCs), we investigated here whether their infection by the neurovirulent MLV FrCasE contributed to neurodegeneration by affecting OPC viability and/or development. Our results show that both neurovirulent and nonneurovirulent MLVs interfere with oligodendrocyte differentiation. Thus, NG2 glial infection could contribute to neurodegeneration by preventing myelin formation and/or repair and by suspending OPCs in a state of persistent susceptibility to excitotoxic insult mediated by neurovirulent virus effects on other glial subtypes.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1128/JVI.03156-15" target="_blank" rel="noreferrer noopener">10.1128/JVI.03156-15</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2016
3T3 Cells
Animals
Cardona Sandra M
Cell Line
Cell Proliferation
Cell Survival
Department of Integrative Medical Sciences
Dunphy Jaclyn M
env/biosynthesis
Female
Gene Products
Journal of virology
Leukemia Virus
Li Ying
Lynch Connor R
Lynch William P
Macklin Wendy B
Male
Mice
Motor Neuron Disease/*virology
Murine/*pathogenicity
NEOMED College of Medicine
Neural Stem Cells/*virology
Neurogenesis/*physiology
Neuroglia/*virology
Oligodendroglia/cytology/virology
Pedraza Carlos E
Retroviridae Infections/*complications
Transgenic
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1152/jn.00227.2014" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/jn.00227.2014</a>
Pages
683–704
Issue
3
Volume
112
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Postinhibitory rebound neurons and networks are disrupted in retrovirus-induced spongiform neurodegeneration.
Publisher
An entity responsible for making the resource available
Journal of neurophysiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
2014-08
Subject
The topic of the resource
Action Potentials/physiology; Animals; Antigens/metabolism; auditory midbrain; Calcium/metabolism; env/metabolism; Experimental/physiopathology; Gene Products; Hearing Loss/physiopathology; Inferior Colliculi/physiopathology/virology; inferior colliculus; Leukemia; Leukemia Virus; Membrane Potentials/physiology; Mice; Microglia/physiology/virology; Murine/*physiology; Neural Pathways/physiopathology; Neurodegenerative Diseases/*physiopathology; Neuroglia/physiology/virology; Neurons/*physiology/virology; Patch-Clamp Techniques; postinhibitory rebound neurons; Proteoglycans/metabolism; Retroviridae Infections/*physiopathology/virology; retrovirus; Tissue Culture Techniques; Tumor Virus Infections/*physiopathology/virology; Voltage-Sensitive Dye Imaging; voltage-sensitive dyes
Creator
An entity primarily responsible for making the resource
Li Ying; Davey Robert A; Sivaramakrishnan Shobhana; Lynch William P
Description
An account of the resource
Certain retroviruses induce progressive spongiform motor neuron disease with features resembling prion diseases and amyotrophic lateral sclerosis. With the neurovirulent murine leukemia virus (MLV) FrCasE, Env protein expression within glia leads to postsynaptic vacuolation, cellular effacement, and neuronal loss in the absence of neuroinflammation. To understand the physiological changes associated with MLV-induced spongiosis, and its neuronal specificity, we employed patch-clamp recordings and voltage-sensitive dye imaging in brain slices of the mouse inferior colliculus (IC), a midbrain nucleus that undergoes extensive spongiosis. IC neurons characterized by postinhibitory rebound firing (PIR) were selectively affected in FrCasE-infected mice. Coincident with Env expression in microglia and in glia characterized by NG2 proteoglycan expression (NG2 cells), rebound neurons (RNs) lost PIR, became hyperexcitable, and were reduced in number. PIR loss and hyperexcitability were reversed by raising internal calcium buffer concentrations in RNs. PIR-initiated rhythmic circuits were disrupted, and spontaneous synchronized bursting and prolonged depolarizations were widespread. Other IC neuron cell types and circuits within the same degenerative environment were unaffected. Antagonists of NMDA and/or AMPA receptors reduced burst firing in the IC but did not affect prolonged depolarizations. Antagonists of L-type calcium channels abolished both bursts and slow depolarizations. IC infection by the nonneurovirulent isogenic virus Friend 57E (Fr57E), whose Env protein is structurally similar to FrCasE, showed no RN hyperactivity or cell loss; however, PIR latency increased. These findings suggest that spongiform neurodegeneration arises from the unique excitability of RNs, their local regulation by glia, and the disruption of this relationship by glial expression of abnormal protein.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/jn.00227.2014" target="_blank" rel="noreferrer noopener">10.1152/jn.00227.2014</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2014
Action Potentials/physiology
Animals
Antigens/metabolism
auditory midbrain
Calcium/metabolism
Davey Robert A
Department of Integrative Medical Sciences
env/metabolism
Experimental/physiopathology
Gene Products
Hearing Loss/physiopathology
Inferior Colliculi/physiopathology/virology
inferior colliculus
Journal of neurophysiology
Leukemia
Leukemia Virus
Li Ying
Lynch William P
Membrane Potentials/physiology
Mice
Microglia/physiology/virology
Murine/*physiology
NEOMED College of Medicine
Neural Pathways/physiopathology
Neurodegenerative Diseases/*physiopathology
Neuroglia/physiology/virology
Neurons/*physiology/virology
Patch-Clamp Techniques
postinhibitory rebound neurons
Proteoglycans/metabolism
Retroviridae Infections/*physiopathology/virology
retrovirus
Sivaramakrishnan Shobhana
Tissue Culture Techniques
Tumor Virus Infections/*physiopathology/virology
Voltage-Sensitive Dye Imaging
voltage-sensitive dyes
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1186/1742-4690-7-93" target="_blank" rel="noreferrer noopener">http://doi.org/10.1186/1742-4690-7-93</a>
Pages
93–93
Volume
7
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Misfolding of CasBrE SU is reversed by interactions with 4070A Env: implications for gammaretroviral neuropathogenesis.
Publisher
An entity responsible for making the resource available
Retrovirology
Date
A point or period of time associated with an event in the lifecycle of the resource
2010
2010-11
Subject
The topic of the resource
Animals; Cell Line; env/*metabolism; Experimental/*virology; Gene Products; Helper Viruses/metabolism/pathogenicity/*physiology; Leukemia; Leukemia Virus; Mice; Motor Neuron Disease/*virology; Murine/metabolism/pathogenicity/*physiology; Neural Stem Cells/*virology; Protein Binding; Protein Folding; Protein Subunits/metabolism; Retroviridae Infections/*virology; Tumor Virus Infections/*virology; Virulence
Creator
An entity primarily responsible for making the resource
Li Ying; Lynch William P
Description
An account of the resource
BACKGROUND: CasBrE is a neurovirulent murine leukemia virus (MLV) capable of inducing paralytic disease with associated spongiform neurodegeneration. The neurovirulence of this virus has been genetically mapped to the surface expressed subunit (SU) of the env gene. However, CasBrE SU synthesized in the absence of the transmembrane subunit (TM) does not retain ecotropic receptor binding activity, indicating that folding of the receptor binding domain (RBD) requires this domain. Using a neural stem cell (NSC) based viral trans complementation approach to examine whether misfolded CasBrE SU retained neurovirulence, we observed CasBrE SU interaction with the "non-neurovirulent" amphotropic helper virus, 4070A which restored functional activity of CasBrE SU. RESULTS: Herein, we show that infection of NSCs expressing CasBrE SU with 4070A (CasES+4070A-NSCs) resulted in the redistribution of CasBrE SU from a strictly secreted product to include retention on the plasma membrane. Cell surface cross-linking analysis suggested that CasBrE SU membrane localization was due to interactions with 4070A Env. Viral particles produced from CasES+4070A-NSCS contained both CasBrE and 4070A gp70 Env proteins. These particles displayed ecotropic receptor-mediated infection, but were still 100-fold less efficient than CasE+4070A-NSC virus. Infectious center analysis showed CasBrE SU ecotropic transduction efficiencies approaching those of NSCs expressing full length CasBrE Env (CasE; SU+TM). In addition, CasBrE SU-4070A Env interactions resulted in robust ecotropic superinfection interference indicating near native intracellular SU interaction with its receptor, mCAT-1. CONCLUSIONS: In this report we provided evidence that 4070A Env and CasBrE SU physically interact within NSCs leading to CasBrE SU retention on the plasma membrane, incorporation into viral particles, restoration of mCAT-1 binding, and capacity for initiation of TM-mediated fusion events. Thus, heterotropic Env-SU interactions facilitates CasBrE SU folding events that restore Env activity. These findings are consistent with the idea that one protein conformation acts as a folding scaffold or nucleus for a second protein of similar primary structure, a process reminiscent of prion formation. The implication is that template-based protein folding may represent an inherent feature of neuropathogenic proteins that extends to retroviral Envs.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1186/1742-4690-7-93" target="_blank" rel="noreferrer noopener">10.1186/1742-4690-7-93</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2010
Animals
Cell Line
Department of Integrative Medical Sciences
env/*metabolism
Experimental/*virology
Gene Products
Helper Viruses/metabolism/pathogenicity/*physiology
Leukemia
Leukemia Virus
Li Ying
Lynch William P
Mice
Motor Neuron Disease/*virology
Murine/metabolism/pathogenicity/*physiology
NEOMED College of Medicine
Neural Stem Cells/*virology
Protein Binding
Protein Folding
Protein Subunits/metabolism
Retroviridae Infections/*virology
Retrovirology
Tumor Virus Infections/*virology
Virulence