58 research outputs found
Self-reactive CD4+ T cells activated during viral-induced demyelination do not prevent clinical recovery
Receptors for Theiler's murine encephalomyelitis virus: characterization by using rabbit antiviral antiserum
Characterization and Specificity of Humoral Immune Responses to Theiler's Murine Encephalomyelitis Virus Capsid Proteins
Monoclonal anti-I-A antibody reverses chronic paralysis and demyelination in Theiler's virus-infected mice: critical importance of timing of treatment
Over-expression of GTP-binding proteins and GTPase activity in mouse astrocyte membranes in response to Theilerâs murine encephalomyelitis virus infection
L* Protein of the DA Strain of Theilerâs Murine Encephalomyelitis Virus Is Important for Virus Growth in a Murine Macrophage-Like Cell Line
Viral Load and a Locus on Chromosome 11 Affect the Late Clinical Disease Caused by Theiler's Virus
International audienceTheiler's virus causes a persistent infection and a demyelinating disease of mice which is a model for multiple sclerosis. Susceptibility to viral persistence maps to several loci, including the interferon gamma locus. Inactivating the gene coding for the interferon gamma receptor makes 129/Sv mice susceptible to persistent infection and clinical disease, whereas inactivating the interferon gamma gene makes C57BL/6 mice susceptible to persistent infection but not to clinical disease. This difference in phenotype is due to the difference in genetic background. Clinical disease depends on high viral load and Tmevd5, a locus on chromosome 11. These results have consequences for the identification of viruses which might be implicated in multiple sclerosis
Early infection of the central nervous system by the GDVII and DA strains of Theiler's virus
Viral Load and a Locus on Chromosome 11 Affect the Late Clinical Disease Caused by Theilerâs Virus
High Numbers of Viral RNA Copies in the Central Nervous System of Mice during Persistent Infection with Theiler's Virus
The low-neurovirulence Theiler's murine encephalomyelitis viruses (TMEV), such as BeAn virus, cause a persistent infection of the central nervous system (CNS) in susceptible mouse strains that results in inflammatory demyelination. The ability of TMEV to persist in the mouse CNS has traditionally been demonstrated by recovering infectious virus from the spinal cord. Results of infectivity assays led to the notion that TMEV persists at low levels. In the present study, we analyzed the copy number of TMEV genomes, plus- to minus-strand ratios, and full-length species in the spinal cords of infected mice and infected tissue culture cells by using Northern hybridization. Considering the low levels of infectious virus in the spinal cord, a surprisingly large number of viral genomes (mean of 3.0 Ă 10(9)) was detected in persistently infected mice. In the transition from the acute (approximately postinfection [p.i.] day 7) to the persistent (beginning on p.i. day 28) phase of infection, viral RNA copy numbers steadily increased, indicating that TMEV persistence involves active viral RNA replication. Further, BeAn viral genomes were full-length in size; i.e., no subgenomic species were detected and the ratio of BeAn virus plus- to minus-strand RNA indicated that viral RNA replication is unperturbed in the mouse spinal cord. Analysis of cultured macrophages and oligodendrocytes suggests that either of these cell types can potentially synthesize high numbers of viral RNA copies if infected in the spinal cord and therefore account for the heavy viral load. A scheme is presented for the direct isolation of both cell types directly from infected spinal cords for further viral analyses
- âŠ