Fibrin deposition in the central nervous system correlates with the degree of Theiler's murine encephalomyelitis virus-induced demyelinating disease

1997 ◽  
Vol 77 (2) ◽  
pp. 185-194 ◽  
Author(s):  
Atsushi Inoue ◽  
Chang-Sung Koh ◽  
Masashi Yamazaki ◽  
Nobuo Yanagisawa ◽  
Yoshihiro Ishihara ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Demyelinating Disease ◽  
Fibrin Deposition ◽  
Theiler's Murine Encephalomyelitis Virus ◽  
Theiler’S Murine Encephalomyelitis Virus ◽  
Encephalomyelitis Virus ◽  
The Central Nervous System

scholarly journals Epitope-Tagged L* Protein of Theiler's Murine Encephalomyelitis Virus Is Expressed in the Central Nervous System in the Acute Phase of Infection

2002 ◽  
Vol 76 (24) ◽  
pp. 13049-13054 ◽  
Author(s):  
Kunihiko Asakura ◽  
Harunobu Murayama ◽  
Toshiki Himeda ◽  
Yoshiro Ohara
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Acute Phase ◽  
Wild Type Virus ◽  
Theiler's Murine Encephalomyelitis Virus ◽  
L Protein ◽  
Theiler’S Murine Encephalomyelitis Virus ◽  
Encephalomyelitis Virus ◽  
The Central Nervous System ◽  
Resistant Strains

ABSTRACT TO subgroup strains of Theiler's murine encephalomyelitis virus (TMEV) synthesize L* protein from an alternative initiation codon. We first demonstrated L* expression in the central nervous system (CNS) of TMEV-infected mice during the acute phase of infection by immunoprecipitation and immunoblotting with anti-L* antibody. In addition, we generated mutant viruses which synthesize FLAG or 3xFLAG epitope-tagged L* protein. With a mutant virus expressing 3xFLAG epitope-tagged L*, designated DA/3xFLAGL*, we investigated L* in the CNS in the acute phase of infection. DA/3xFLAGL* did not change the virus tropism in comparison with wild-type virus, and L* was clearly identified in the CNS in both susceptible and resistant strains of mice. Double immunolabeling studies showed that L* is colocalized with TMEV polyprotein and exclusively expressed in neurons.

scholarly journals CD154 Blockade Results in Transient Reduction in Theiler's Murine Encephalomyelitis Virus-Induced Demyelinating Disease

2003 ◽  
Vol 77 (3) ◽  
pp. 2247-2250 ◽  
Author(s):  
Laurence M. Howard ◽  
Katherine L. Neville ◽  
Lia M. Haynes ◽  
Mauro C. Dal Canto ◽  
Stephen D. Miller
Keyword(s):  
Central Nervous System ◽  
Immune Cell ◽  
Demyelinating Disease ◽  
Immune Cell Infiltration ◽  
Theiler's Murine Encephalomyelitis Virus ◽  
Viral Loads ◽  
Theiler’S Murine Encephalomyelitis Virus ◽  
Cell Responses ◽  
Encephalomyelitis Virus ◽  
The Central Nervous System

ABSTRACT Transient CD154 blockade at the onset of Theiler's murine encephalomyelitis virus-induced demyelinating disease ameliorated disease progression for 80 days, reduced immune cell infiltration, and transiently increased viral loads in the central nervous system. Peripheral antiviral and autoimmune T-cell responses were normal, and disease severity returned to control levels by day 120.

scholarly journals A Determinant for Central Nervous System Persistence Localized in the Capsid of Theiler’s Murine Encephalomyelitis Virus by Using Recombinant Viruses

1998 ◽  
Vol 72 (2) ◽  
pp. 1662-1665 ◽  
Author(s):  
Cecilia Adami ◽  
Arthur E. Pritchard ◽  
Todd Knauf ◽  
Ming Luo ◽  
Howard L. Lipton
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Close Contact ◽  
Theiler's Murine Encephalomyelitis Virus ◽  
Recombinant Viruses ◽  
Theiler’S Murine Encephalomyelitis Virus ◽  
Conformational Determinant ◽  
Encephalomyelitis Virus ◽  
The Central Nervous System ◽  
Loop Regions

ABSTRACT The demyelinating process in Theiler’s murine encephalomyelitis virus (TMEV) infection in mice requires virus persistence in the central nervous system. Using recombinant TMEV assembled between the virulent GDVII and less virulent BeAn virus cDNAs, we now provide additional evidence supporting the localization of a persistence determinant to the leader P1 (capsid) sequences. Further, recombinant viruses in which BeAn sequences progressively replaced those of GDVII within the capsid starting at the leader NH2 terminus suggest that a conformational determinant requiring homologous sequences in both the VP2 puff and VP1 loop regions, which are in close contact on the virion surface, might underlie persistence.

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